Wunki HBF3 Exam 2 Endocrine Pancreas PDF

#separator:tab #html:true "Glucose HomeostasisBlood glucose levels are maintained at [...] mg/dL. Insulin is secreted in response to high blood glucose and stimulates absorption and storage of glucose. Glucagon is secreted in response to low blood glucose and stimulates glucose synthesis by the live...

#separator:tab #html:true "Glucose HomeostasisBlood glucose levels are maintained at [...] mg/dL. Insulin is secreted in response to high blood glucose and stimulates absorption and storage of glucose. Glucagon is secreted in response to low blood glucose and stimulates glucose synthesis by the liver. " "Glucose HomeostasisBlood glucose levels are maintained at 100 mg/dL. Insulin is secreted in response to high blood glucose and stimulates absorption and storage of glucose. Glucagon is secreted in response to low blood glucose and stimulates glucose synthesis by the liver.  Review - suspend if desired" "Glucose HomeostasisBlood glucose levels are maintained at 100 mg/dL. [...] is secreted in response to high blood glucose and stimulates absorption and storage of glucose. [...] is secreted in response to low blood glucose and stimulates glucose synthesis by the liver. " "Glucose HomeostasisBlood glucose levels are maintained at 100 mg/dL. Insulin is secreted in response to high blood glucose and stimulates absorption and storage of glucose. Glucagon is secreted in response to low blood glucose and stimulates glucose synthesis by the liver.  Review - suspend if desired" "Pancreatic HormonesThe major hormones produced by the islets of Langerhans are:- [...] from alpha cells- [...] from beta cells- [...] from delta (D) cells" "Pancreatic HormonesThe major hormones produced by the islets of Langerhans are:- Glucagon from alpha cells- Insulin from beta cells- Somatostatin from delta (D) cells " "Regulation of Insulin ReleasePhases of insulin secretion:1. [...]: PANS-mediated2. Early [...]: incretin-mediated3. [...]: mediated by levels of blood glucose" "Regulation of Insulin ReleasePhases of insulin secretion:1. Cephalic: PANS-mediated2. Early postprandial: incretin-mediated3. Postprandial: mediated by levels of blood glucose " "Regulation of Insulin ReleasePhases of insulin secretion:1. Cephalic: [...]-mediated2. Early postprandial: [...]-mediated3. Postprandial: mediated by levels of [...]" "Regulation of Insulin ReleasePhases of insulin secretion:1. Cephalic: PANS-mediated2. Early postprandial: incretin-mediated3. Postprandial: mediated by levels of blood glucose " "Regulation of Insulin ReleaseThe incretins ([...] and [...]) are peptide hormones produced by L-cells in the lining of the gut. They are secreted into the bloodstream shortly after food enters the gut lumen and act on the pancreas to enhance insulin secretion." "Regulation of Insulin ReleaseThe incretins (GLP1 and GIP) are peptide hormones produced by L-cells in the lining of the gut. They are secreted into the bloodstream shortly after food enters the gut lumen and act on the pancreas to enhance insulin secretion. " "Regulation of Insulin ReleaseThe [...] (GLP1 and GIP) are peptide hormones produced by [...]-cells in the lining of the gut. They are secreted into the bloodstream shortly after food enters the gut lumen and act on the pancreas to [enhance/suppress] insulin secretion." "Regulation of Insulin ReleaseThe incretins (GLP1 and GIP) are peptide hormones produced by L-cells in the lining of the gut. They are secreted into the bloodstream shortly after food enters the gut lumen and act on the pancreas to enhance insulin secretion. " "Regulation of Insulin ReleaseThe incretins (GLP1 and GIP) are [...] hormones produced by L-cells in the lining of the [...]. They are secreted into the bloodstream shortly after food enters the [...] lumen and act on the pancreas to enhance insulin secretion." "Regulation of Insulin ReleaseThe incretins (GLP1 and GIP) are peptide hormones produced by L-cells in the lining of the gut. They are secreted into the bloodstream shortly after food enters the gut lumen and act on the pancreas to enhance insulin secretion. " "Regulation of Insulin ReleaseIncreases in blood glucose produce [...] increases in [...] because intracellular glucose metabolism is linked directly to [...] exocytosis. " "Regulation of Insulin ReleaseIncreases in blood glucose produce proportional increases in insulin because intracellular glucose metabolism is linked directly to insulin exocytosis.  " "Regulation of Insulin ReleaseSteps for insulin release in beta islet cells:1. Glucose enters the cell via GLUT22. Glucose metabolism produces ATP3. ATP inhibits K+ channels, producing depolarization of the cell 4. Depolarization of the cell causes [...] influx5. Increase in intracellular [...] causes exocytosis of insulin secretory granules" "Regulation of Insulin ReleaseSteps for insulin release in beta islet cells:1. Glucose enters the cell via GLUT22. Glucose metabolism produces ATP3. ATP inhibits K+ channels, producing depolarization of the cell 4. Depolarization of the cell causes Ca++ influx5. Increase in intracellular Ca++ causes exocytosis of insulin secretory granules " "Regulation of Insulin ReleaseSteps for insulin release in beta islet cells:1. Glucose enters the cell via [...]2. Glucose metabolism produces [...]3. ATP inhibits K+ channels, producing depolarization of the cell 4. Depolarization of the cell causes Ca++ influx5. Increase in intracellular Ca++ causes exocytosis of insulin secretory granules" "Regulation of Insulin ReleaseSteps for insulin release in beta islet cells:1. Glucose enters the cell via GLUT22. Glucose metabolism produces ATP3. ATP inhibits K+ channels, producing depolarization of the cell 4. Depolarization of the cell causes Ca++ influx5. Increase in intracellular Ca++ causes exocytosis of insulin secretory granules " "Regulation of Insulin ReleaseSteps for insulin release in beta islet cells:1. Glucose enters the cell via GLUT22. Glucose metabolism produces ATP3. ATP inhibits [...] channels, producing [...] of the cell 4. [...] of the cell causes Ca++ influx5. Increase in intracellular Ca++ causes exocytosis of insulin secretory granules" "Regulation of Insulin ReleaseSteps for insulin release in beta islet cells:1. Glucose enters the cell via GLUT22. Glucose metabolism produces ATP3. ATP inhibits K+ channels, producing depolarization of the cell 4. Depolarization of the cell causes Ca++ influx5. Increase in intracellular Ca++ causes exocytosis of insulin secretory granules " "Regulation of Insulin ReleaseSteps for insulin release in beta islet cells:1. Glucose enters the cell via GLUT22. Glucose metabolism produces ATP3. ATP inhibits K+ channels, producing depolarization of the cell 4. Depolarization of the cell causes Ca++ influx5. Increase in intracellular Ca++ causes [...] of insulin secretory granules" "Regulation of Insulin ReleaseSteps for insulin release in beta islet cells:1. Glucose enters the cell via GLUT22. Glucose metabolism produces ATP3. ATP inhibits K+ channels, producing depolarization of the cell 4. Depolarization of the cell causes Ca++ influx5. Increase in intracellular Ca++ causes exocytosis of insulin secretory granules " "Regulation of Insulin ReleaseOther modulators (neural and hormonal) of insulin secretion act via the [...] pathway and the [...] pathway and either promote or inhibit vesicle fusion." "Regulation of Insulin ReleaseOther modulators (neural and hormonal) of insulin secretion act via the cAMP/PKA pathway and the PLC pathway and either promote or inhibit vesicle fusion. " "Insulin SynthesisInsulin is initially produced as preproinsulin, which is then converted to [...]. Proteolysis of [...] produces insulin and [...]." "Insulin SynthesisInsulin is initially produced as preproinsulin, which is then converted to proinsulin. Proteolysis of proinsulin produces insulin and C peptide. " "Insulin SynthesisInsulin is initially produced as [...], which is then converted to proinsulin. [...] of proinsulin produces [...] and C peptide." "Insulin SynthesisInsulin is initially produced as preproinsulin, which is then converted to proinsulin. Proteolysis of proinsulin produces insulin and C peptide. " "Insulin ActionInsulin [...] anabolism, [...] catabolism, and alters [...]." "Insulin ActionInsulin stimulates anabolism, antagonizes catabolism, and alters electrolyte balance. Insulin acts through a tyrosine kinase receptor" "Insulin Action1. Stimulates anabolism: Insulin acts to [increase/decrease] the cellular uptake of glucose, fatty acids and amino acids, and stimulates their conversion into glycogen, triglyceride, and protein." "Insulin Action1. Stimulates anabolism: Insulin acts to increase the cellular uptake of glucose, fatty acids and amino acids, and stimulates their conversion into glycogen, triglyceride, and protein. " "Insulin Action1. Stimulates anabolism: Insulin acts to increase the cellular uptake of glucose, fatty acids and amino acids, and stimulates their conversion into [...], [...], and protein." "Insulin Action1. Stimulates anabolism: Insulin acts to increase the cellular uptake of glucose, fatty acids and amino acids, and stimulates their conversion into glycogen, triglyceride, and protein. " "Insulin Action2. Antagonizes catabolism: Insulin [increases/decreases] glycogenolysis, lipolysis and proteolysis. In addition, it [stimulates/suppresses] hepatic gluconeogenesis." "Insulin Action2. Antagonizes catabolism: Insulin decreases glycogenolysis, lipolysis and proteolysis. In addition, it suppresses hepatic gluconeogenesis. " "Insulin Action2. Antagonizes catabolism: Insulin decreases glycogenolysis, lipolysis and proteolysis. In addition, it suppresses hepatic [...]." "Insulin Action2. Antagonizes catabolism: Insulin decreases glycogenolysis, lipolysis and proteolysis. In addition, it suppresses hepatic gluconeogenesis. " "Insulin Action2. Antagonizes catabolism: Insulin decreases [...], [...] and proteolysis. In addition, it suppresses hepatic gluconeogenesis." "Insulin Action2. Antagonizes catabolism: Insulin decreases glycogenolysis, lipolysis and proteolysis. In addition, it suppresses hepatic gluconeogenesis. " "Insulin Action3. Alters electrolyte balance: Insulin increases the cellular uptake of potassium and phosphate and [increases/decreases] the cellular uptake of sodium and calcium" "Insulin Action3. Alters electrolyte balance: Insulin increases the cellular uptake of potassium and phosphate and decreases the cellular uptake of sodium and calcium " "Insulin Action3. Alters electrolyte balance: Insulin [increases/decreases] the cellular uptake of potassium and phosphate and decreases the cellular uptake of sodium and calcium" "Insulin Action3. Alters electrolyte balance: Insulin increases the cellular uptake of potassium and phosphate and decreases the cellular uptake of sodium and calcium " "Insulin Action3. Alters electrolyte balance: Insulin increases the cellular uptake of [...] and [...] and decreases the cellular uptake of sodium and calcium" "Insulin Action3. Alters electrolyte balance: Insulin increases the cellular uptake of potassium and phosphate and decreases the cellular uptake of sodium and calcium " "Insulin Action3. Alters electrolyte balance: Insulin increases the cellular uptake of potassium and phosphate and decreases the cellular uptake of [...] and [...]" "Insulin Action3. Alters electrolyte balance: Insulin increases the cellular uptake of potassium and phosphate and decreases the cellular uptake of sodium and calcium " "Insulin SignalingInsulin acts by binding at a [...] receptor on the cell surface. The downstream effects of insulin differ from tissue to tissue, but a common step is the phosphorylation of an [...] protein. This protein then serves as a docking site for additional intracellular signaling proteins" "Insulin SignalingInsulin acts by binding at a tyrosine kinase receptor on the cell surface. The downstream effects of insulin differ from tissue to tissue, but a common step is the phosphorylation of an IRS (insulin receptor substrate) protein. This protein then serves as a docking site for additional intracellular signaling proteins " "Insulin SignalingA branch of the insulin signaling network of importance to metabolic regulation is the IRS/PI3K/AKT pathway. This pathway is responsible for mediating insulin’s effects on [...] (by activating GLUT4) and [...] (by inhibiting the kinase that inactivates glycogen synthase)." "Insulin SignalingA branch of the insulin signaling network of importance to metabolic regulation is the IRS/PI3K/AKT pathway. This pathway is responsible for mediating insulin’s effects on glucose uptake (by activating GLUT4) and glycogen synthesis (by inhibiting the kinase that inactivates glycogen synthase). " "Insulin SignalingA branch of the insulin signaling network of importance to metabolic regulation is the IRS/PI3K/AKT pathway. This pathway is responsible for mediating insulin’s effects on glucose uptake (by activating [...]) and glycogen synthesis (by inhibiting the kinase that inactivates [...])." "Insulin SignalingA branch of the insulin signaling network of importance to metabolic regulation is the IRS/PI3K/AKT pathway. This pathway is responsible for mediating insulin’s effects on glucose uptake (by activating GLUT4) and glycogen synthesis (by inhibiting the kinase that inactivates glycogen synthase). " "Insulin EffectsThe overall effect of postprandial insulin is to convert circulating diet-derived glucose into [...] and [...] stored in muscle, liver and adipose tissue. This is accomplished by increasing glucose uptake into these tissues, stimulating glycogen synthesis in skeletal muscle and liver, and stimulating lipogenesis in liver and adipose tissue." "Insulin EffectsThe overall effect of postprandial insulin is to convert circulating diet-derived glucose into glycogen and triglyceride stored in muscle, liver and adipose tissue. This is accomplished by increasing glucose uptake into these tissues, stimulating glycogen synthesis in skeletal muscle and liver, and stimulating lipogenesis in liver and adipose tissue. " "Insulin EffectsThe overall effect of postprandial insulin is to convert circulating diet-derived glucose into glycogen and triglyceride stored in muscle, liver and adipose tissue. This is accomplished by increasing [...] into these tissues, stimulating [...] in skeletal muscle and liver, and stimulating lipogenesis in liver and adipose tissue." "Insulin EffectsThe overall effect of postprandial insulin is to convert circulating diet-derived glucose into glycogen and triglyceride stored in muscle, liver and adipose tissue. This is accomplished by increasing glucose uptake into these tissues, stimulating glycogen synthesis in skeletal muscle and liver, and stimulating lipogenesis in liver and adipose tissue. " "Insulin EffectsThe overall effect of postprandial insulin is to convert circulating diet-derived glucose into glycogen and triglyceride stored in muscle, liver and adipose tissue. This is accomplished by increasing glucose uptake into these tissues, stimulating glycogen synthesis in skeletal muscle and liver, and stimulating [...] in liver and adipose tissue." "Insulin EffectsThe overall effect of postprandial insulin is to convert circulating diet-derived glucose into glycogen and triglyceride stored in muscle, liver and adipose tissue. This is accomplished by increasing glucose uptake into these tissues, stimulating glycogen synthesis in skeletal muscle and liver, and stimulating lipogenesis in liver and adipose tissue. " "Insulin EffectsAlthough the [...] does not respond to insulin, it plays an important role in whole-body glucose homeostasis. This is because the [...] depends on glucose for fuel and uses it in large amounts, but cannot store it." "Insulin EffectsAlthough the brain does not respond to insulin, it plays an important role in whole-body glucose homeostasis. This is because the brain depends on glucose for fuel and uses it in large amounts, but cannot store it. " "Insulin EffectsThe primary effects of insulin in the [...] are suppression of glucose output and stimulation of glycogen synthesis. Additionally, insulin promotes the synthesis and storage of [...], and can stimulate the release of excess lipid into circulation as VLDL. Finally, by mechanisms that are not well understood, insulin promotes protein synthesis and inhibits protein breakdown." "Insulin EffectsThe primary effects of insulin in the liver are suppression of glucose output and stimulation of glycogen synthesis. Additionally, insulin promotes the synthesis and storage of fats, and can stimulate the release of excess lipid into circulation as VLDL. Finally, by mechanisms that are not well understood, insulin promotes protein synthesis and inhibits protein breakdown. " "Insulin EffectsThe primary effects of insulin in the liver are [...] of glucose output and [...] of glycogen synthesis. Additionally, insulin promotes the synthesis and storage of fats, and can stimulate the release of excess lipid into circulation as VLDL. Finally, by mechanisms that are not well understood, insulin promotes protein synthesis and inhibits protein breakdown." "Insulin EffectsThe primary effects of insulin in the liver are suppression of glucose output and stimulation of glycogen synthesis. Additionally, insulin promotes the synthesis and storage of fats, and can stimulate the release of excess lipid into circulation as VLDL. Finally, by mechanisms that are not well understood, insulin promotes protein synthesis and inhibits protein breakdown. " "Insulin EffectsThe primary effects of insulin in the liver are suppression of glucose output and stimulation of glycogen synthesis. Additionally, insulin promotes the synthesis and storage of fats, and can stimulate the release of excess lipid into circulation as [...]. Finally, by mechanisms that are not well understood, insulin promotes protein [...] and inhibits protein [...]." "Insulin EffectsThe primary effects of insulin in the liver are suppression of glucose output and stimulation of glycogen synthesis. Additionally, insulin promotes the synthesis and storage of fats, and can stimulate the release of excess lipid into circulation as VLDL. Finally, by mechanisms that are not well understood, insulin promotes protein synthesis and inhibits protein breakdown. " "Insulin EffectsThe primary effects of insulin in the liver are suppression of [...] output and stimulation of [...] synthesis. Additionally, insulin promotes the synthesis and storage of fats, and can stimulate the release of excess lipid into circulation as VLDL. Finally, by mechanisms that are not well understood, insulin promotes protein synthesis and inhibits protein breakdown." "Insulin EffectsThe primary effects of insulin in the liver are suppression of glucose output and stimulation of glycogen synthesis. Additionally, insulin promotes the synthesis and storage of fats, and can stimulate the release of excess lipid into circulation as VLDL. Finally, by mechanisms that are not well understood, insulin promotes protein synthesis and inhibits protein breakdown. " "Insulin EffectsTo mediate glucose metabolism in the liver, insulin enhances glucokinase and suppresses G6Pase to ensure that all the glucose entering the cell is phosphorylated, which prevents its re-release back into circulation. Insulin also stimulates glycogen synthase and inhibits glycogen phosphorylase to drive the conversion of glucose to glycogen (glycogenesis). Insulin also inhibits gluconeogenesis by reducing the amount of [...], [...], and G6Pase." "Insulin EffectsTo mediate glucose metabolism in the liver, insulin enhances glucokinase and suppresses G6Pase to ensure that all the glucose entering the cell is phosphorylated, which prevents its re-release back into circulation. Insulin also stimulates glycogen synthase and inhibits glycogen phosphorylase to drive the conversion of glucose to glycogen (glycogenesis). Insulin also inhibits gluconeogenesis by reducing the amount of PEPCK, FBPase, and G6Pase. " "Insulin EffectsTo mediate glucose metabolism in the liver, insulin enhances glucokinase and suppresses G6Pase to ensure that all the glucose entering the cell is phosphorylated, which prevents its re-release back into circulation. Insulin also stimulates [...] and inhibits [...] to drive the conversion of glucose to glycogen (glycogenesis). Insulin also inhibits gluconeogenesis by reducing the amount of PEPCK, FBPase, and G6Pase." "Insulin EffectsTo mediate glucose metabolism in the liver, insulin enhances glucokinase and suppresses G6Pase to ensure that all the glucose entering the cell is phosphorylated, which prevents its re-release back into circulation. Insulin also stimulates glycogen synthase and inhibits glycogen phosphorylase to drive the conversion of glucose to glycogen (glycogenesis). Insulin also inhibits gluconeogenesis by reducing the amount of PEPCK, FBPase, and G6Pase. " "Insulin EffectsTo mediate glucose metabolism in the liver, insulin enhances [...] and suppresses [...] to ensure that all the glucose entering the cell is phosphorylated, which prevents its re-release back into circulation. Insulin also stimulates glycogen synthase and inhibits glycogen phosphorylase to drive the conversion of glucose to glycogen (glycogenesis). Insulin also inhibits gluconeogenesis by reducing the amount of PEPCK, FBPase, and [...]." "Insulin EffectsTo mediate glucose metabolism in the liver, insulin enhances glucokinase and suppresses G6Pase to ensure that all the glucose entering the cell is phosphorylated, which prevents its re-release back into circulation. Insulin also stimulates glycogen synthase and inhibits glycogen phosphorylase to drive the conversion of glucose to glycogen (glycogenesis). Insulin also inhibits gluconeogenesis by reducing the amount of PEPCK, FBPase, and G6Pase. " "Insulin EffectsTo mediate glucose metabolism in the liver, insulin enhances glucokinase and suppresses G6Pase to ensure that all the glucose entering the cell is [...], which prevents its re-release back into circulation. Insulin also stimulates glycogen synthase and inhibits glycogen phosphorylase to drive the conversion of glucose to glycogen (glycogenesis). Insulin also inhibits gluconeogenesis by reducing the amount of PEPCK, FBPase, and G6Pase." "Insulin EffectsTo mediate glucose metabolism in the liver, insulin enhances glucokinase and suppresses G6Pase to ensure that all the glucose entering the cell is phosphorylated, which prevents its re-release back into circulation. Insulin also stimulates glycogen synthase and inhibits glycogen phosphorylase to drive the conversion of glucose to glycogen (glycogenesis). Insulin also inhibits gluconeogenesis by reducing the amount of PEPCK, FBPase, and G6Pase. " "Insulin EffectsIn [...] and adipose tissue, insulin mediates glucose uptake and does this by recruiting GLUT4 transporters to the plasma membrane. These tissues are the main sites of dietary glucose absorption.In [...] tissue, insulin promote glycogen synthesis through the same pathways it uses in the liver. In adipose tissue, the products of glucose breakdown are used to synthesize [...]." "Insulin EffectsIn muscle and adipose tissue, insulin mediates glucose uptake and does this by recruiting GLUT4 transporters to the plasma membrane. These tissues are the main sites of dietary glucose absorption.In muscle tissue, insulin promote glycogen synthesis through the same pathways it uses in the liver. In adipose tissue, the products of glucose breakdown are used to synthesize fatty acids. " "Insulin EffectsIn muscle and [...] tissue, insulin mediates glucose uptake and does this by recruiting GLUT4 transporters to the plasma membrane. These tissues are the main sites of dietary glucose absorption.In muscle tissue, insulin promote glycogen synthesis through the same pathways it uses in the liver. In [...] tissue, the products of glucose breakdown are used to synthesize fatty acids." "Insulin EffectsIn muscle and adipose tissue, insulin mediates glucose uptake and does this by recruiting GLUT4 transporters to the plasma membrane. These tissues are the main sites of dietary glucose absorption.In muscle tissue, insulin promote glycogen synthesis through the same pathways it uses in the liver. In adipose tissue, the products of glucose breakdown are used to synthesize fatty acids. " "Insulin EffectsIn muscle and adipose tissue, insulin mediates glucose uptake and does this by recruiting [...] transporters to the plasma membrane. These tissues are the main sites of dietary glucose absorption.In muscle tissue, insulin promote glycogen synthesis through the same pathways it uses in the liver. In adipose tissue, the products of glucose breakdown are used to synthesize fatty acids." "Insulin EffectsIn muscle and adipose tissue, insulin mediates glucose uptake and does this by recruiting GLUT4 transporters to the plasma membrane. These tissues are the main sites of dietary glucose absorption.In muscle tissue, insulin promote glycogen synthesis through the same pathways it uses in the liver. In adipose tissue, the products of glucose breakdown are used to synthesize fatty acids. " "Insulin EffectsIn adipose tissue, insulin promotes storage of [...] in triglycerides by inhibiting hormone-sensitive triglyceride lipase, which would break down triglycerides, and promoting the synthesis of lipoprotein lipase. Lipoprotein lipase then frees [...] from chylomicrons and VLDL's in the bloodstream for triglyceride storage in the adipocyte." "Insulin EffectsIn adipose tissue, insulin promotes storage of fatty acids in triglycerides by inhibiting hormone-sensitive triglyceride lipase, which would break down triglycerides, and promoting the synthesis of lipoprotein lipase. Lipoprotein lipase then frees fatty acids from chylomicrons and VLDL's in the bloodstream for triglyceride storage in the adipocyte. In addition to increasing glucose uptake via GLUT4" "Insulin EffectsIn adipose tissue, insulin promotes storage of fatty acids in triglycerides by inhibiting [...], which would break down triglycerides, and promoting the synthesis of [...]. [...] then frees fatty acids from chylomicrons and VLDL's in the bloodstream for triglyceride storage in the adipocyte." "Insulin EffectsIn adipose tissue, insulin promotes storage of fatty acids in triglycerides by inhibiting hormone-sensitive triglyceride lipase, which would break down triglycerides, and promoting the synthesis of lipoprotein lipase. Lipoprotein lipase then frees fatty acids from chylomicrons and VLDL's in the bloodstream for triglyceride storage in the adipocyte. In addition to increasing glucose uptake via GLUT4" "Insulin EffectsIn adipose tissue, insulin promotes storage of fatty acids in triglycerides by [...] hormone-sensitive triglyceride lipase, which would break down triglycerides, and [...] the synthesis of lipoprotein lipase. Lipoprotein lipase then frees fatty acids from chylomicrons and VLDL's in the bloodstream for triglyceride storage in the adipocyte." "Insulin EffectsIn adipose tissue, insulin promotes storage of fatty acids in triglycerides by inhibiting hormone-sensitive triglyceride lipase, which would break down triglycerides, and promoting the synthesis of lipoprotein lipase. Lipoprotein lipase then frees fatty acids from chylomicrons and VLDL's in the bloodstream for triglyceride storage in the adipocyte. In addition to increasing glucose uptake via GLUT4" "Insulin EffectsIn adipose tissue, insulin promotes storage of fatty acids in triglycerides by inhibiting hormone-sensitive triglyceride lipase, which would break down triglycerides, and promoting the synthesis of lipoprotein lipase. Lipoprotein lipase then frees fatty acids from [...] and [...] in the bloodstream for triglyceride storage in the adipocyte." "Insulin EffectsIn adipose tissue, insulin promotes storage of fatty acids in triglycerides by inhibiting hormone-sensitive triglyceride lipase, which would break down triglycerides, and promoting the synthesis of lipoprotein lipase. Lipoprotein lipase then frees fatty acids from chylomicrons and VLDL's in the bloodstream for triglyceride storage in the adipocyte. In addition to increasing glucose uptake via GLUT4" "Glucagon ProductionGlucagon is produced by [...] cells, which are located mostly on the [...] of the islets and constitute 5-20% of the islet cells. Glucagon is initially produced as preproglucagon, which is processed in the pancreas to produce the active 29 aa peptide. That same preproglucagon peptide is cleaved differently in intestinal L cells to produce GLP1 and GLP2." "Glucagon ProductionGlucagon is produced by alpha cells, which are located mostly on the outer mantle of the islets and constitute 5-20% of the islet cells. Glucagon is initially produced as preproglucagon, which is processed in the pancreas to produce the active 29 aa peptide. That same preproglucagon peptide is cleaved differently in intestinal L cells to produce GLP1 and GLP2. GLP: glucagon-like proteins" "Glucagon ProductionGlucagon is produced by alpha cells, which are located mostly on the outer mantle of the islets and constitute 5-20% of the islet cells. Glucagon is initially produced as [...], which is processed in the pancreas to produce the active 29 aa peptide. That same [...] peptide is cleaved differently in intestinal L cells to produce GLP1 and GLP2." "Glucagon ProductionGlucagon is produced by alpha cells, which are located mostly on the outer mantle of the islets and constitute 5-20% of the islet cells. Glucagon is initially produced as preproglucagon, which is processed in the pancreas to produce the active 29 aa peptide. That same preproglucagon peptide is cleaved differently in intestinal L cells to produce GLP1 and GLP2. GLP: glucagon-like proteins" "Glucagon RegulationGlucagon is primarily regulated by the serum levels of glucose, [...], and fatty acids, making its rate of secretion directly linked to the metabolism of carbohydrates, proteins, and fats.Gluocse and fatty acids inhibit glucagon secretion, while [...] stimulate secretion." "Glucagon RegulationGlucagon is primarily regulated by the serum levels of glucose, amino acids, and fatty acids, making its rate of secretion directly linked to the metabolism of carbohydrates, proteins, and fats.Gluocse and fatty acids inhibit glucagon secretion, while amino acids stimulate secretion. " "Glucagon RegulationGlucagon is primarily regulated by the serum levels of glucose, amino acids, and fatty acids, making its rate of secretion directly linked to the metabolism of carbohydrates, proteins, and fats.Gluocse and fatty acids [...] glucagon secretion, while amino acids [...] secretion." "Glucagon RegulationGlucagon is primarily regulated by the serum levels of glucose, amino acids, and fatty acids, making its rate of secretion directly linked to the metabolism of carbohydrates, proteins, and fats.Gluocse and fatty acids inhibit glucagon secretion, while amino acids stimulate secretion. " "Glucagon RegulationGlucagon is primarily regulated by the serum levels of [...], amino acids, and [...], making its rate of secretion directly linked to the metabolism of carbohydrates, proteins, and fats.[...] and [...] inhibit glucagon secretion, while amino acids stimulate secretion." "Glucagon RegulationGlucagon is primarily regulated by the serum levels of glucose, amino acids, and fatty acids, making its rate of secretion directly linked to the metabolism of carbohydrates, proteins, and fats.Gluocse and fatty acids inhibit glucagon secretion, while amino acids stimulate secretion. " "Glucagon RegulationIn addition to nutritional signals, glucagon secretion can be affected by sensory stimulation (e.g. loud noise, pain), and by activation of α-adrenergic signaling. [...] and [...] signaling both stimulate glucagon secretion." "Glucagon RegulationIn addition to nutritional signals, glucagon secretion can be affected by sensory stimulation (e.g. loud noise, pain), and by activation of α-adrenergic signaling. SANS and PANS signaling both stimulate glucagon secretion. " "Glucagon RegulationIn addition to nutritional signals, glucagon secretion can be affected by [...] (e.g. loud noise, pain), and by activation of [...] signaling. SANS and PANS signaling both stimulate glucagon secretion." "Glucagon RegulationIn addition to nutritional signals, glucagon secretion can be affected by sensory stimulation (e.g. loud noise, pain), and by activation of α-adrenergic signaling. SANS and PANS signaling both stimulate glucagon secretion. " "Glucagon RegulationThe secretion of glucagon is also stimulated by a reduction in the level of [...] in the serum. Since glucagon increases the concentration of glucose and [...] in the serum and decreases that of amino acids, it induces a feedback regulation of its own secretion." "Glucagon RegulationThe secretion of glucagon is also stimulated by a reduction in the level of fatty acids in the serum. Since glucagon increases the concentration of glucose and fatty acids in the serum and decreases that of amino acids, it induces a feedback regulation of its own secretion. " "Glucagon RegulationThe secretion of glucagon is also stimulated by a reduction in the level of fatty acids in the serum. Since glucagon increases the concentration of [...] and fatty acids in the serum and decreases that of [...], it induces a feedback regulation of its own secretion." "Glucagon RegulationThe secretion of glucagon is also stimulated by a reduction in the level of fatty acids in the serum. Since glucagon increases the concentration of glucose and fatty acids in the serum and decreases that of amino acids, it induces a feedback regulation of its own secretion. " "Glucagon EffectsGlucagon stimulates [...] and [...] in the liver to increase overall glucose output. In adipose tissue, it stimulates lipolysis. Through these effects on the liver and fat, glucagon increases levels of glucose and fatty acids." "Glucagon EffectsGlucagon stimulates gluconeogenesis and glycogenolysis in the liver to increase overall glucose output. In adipose tissue, it stimulates lipolysis. Through these effects on the liver and fat, glucagon increases levels of glucose and fatty acids. " "Glucagon EffectsGlucagon stimulates gluconeogenesis and glycogenolysis in the liver to increase overall glucose output. In adipose tissue, it stimulates [...]. Through these effects on the liver and fat, glucagon increases levels of glucose and [...]." "Glucagon EffectsGlucagon stimulates gluconeogenesis and glycogenolysis in the liver to increase overall glucose output. In adipose tissue, it stimulates lipolysis. Through these effects on the liver and fat, glucagon increases levels of glucose and fatty acids. " "Glucagon EffectsIn the liver, glucagon acts through a GPCR cAMP/PKA pathway to stimulate the production and release of glucose through activating gluconeogenesis and glycogenolysis. Glucagon also inhibits glycolysis and lipogenesis which has a glucose sparing effect. Glucagon stimulates fatty acid oxidation, which produces ATP to meet the energy demands of the cells. Finally, glucagon stimulates the uptake of amino acids by the liver, which are used as substrates for gluconeogenesis. Thus, glucagon converts the liver from an organ of glucose [...] to an organ of glucose [...]." "Glucagon EffectsIn the liver, glucagon acts through a GPCR cAMP/PKA pathway to stimulate the production and release of glucose through activating gluconeogenesis and glycogenolysis. Glucagon also inhibits glycolysis and lipogenesis which has a glucose sparing effect. Glucagon stimulates fatty acid oxidation, which produces ATP to meet the energy demands of the cells. Finally, glucagon stimulates the uptake of amino acids by the liver, which are used as substrates for gluconeogenesis. Thus, glucagon converts the liver from an organ of glucose storage to an organ of glucose production. " "Glucagon EffectsIn the liver, glucagon acts through a GPCR cAMP/PKA pathway to stimulate the production and release of glucose through activating gluconeogenesis and glycogenolysis. Glucagon also inhibits glycolysis and lipogenesis which has a glucose sparing effect. Glucagon stimulates fatty acid oxidation, which produces ATP to meet the energy demands of the cells. Finally, glucagon stimulates the uptake of [...] by the liver, which are used as substrates for [...]. Thus, glucagon converts the liver from an organ of glucose storage to an organ of glucose production." "Glucagon EffectsIn the liver, glucagon acts through a GPCR cAMP/PKA pathway to stimulate the production and release of glucose through activating gluconeogenesis and glycogenolysis. Glucagon also inhibits glycolysis and lipogenesis which has a glucose sparing effect. Glucagon stimulates fatty acid oxidation, which produces ATP to meet the energy demands of the cells. Finally, glucagon stimulates the uptake of amino acids by the liver, which are used as substrates for gluconeogenesis. Thus, glucagon converts the liver from an organ of glucose storage to an organ of glucose production. " "Glucagon EffectsIn the liver, glucagon acts through a GPCR cAMP/PKA pathway to stimulate the production and release of glucose through activating gluconeogenesis and glycogenolysis. Glucagon also [...] glycolysis and lipogenesis which has a glucose sparing effect. Glucagon stimulates [...], which produces ATP to meet the energy demands of the cells. Finally, glucagon stimulates the uptake of amino acids by the liver, which are used as substrates for gluconeogenesis. Thus, glucagon converts the liver from an organ of glucose storage to an organ of glucose production." "Glucagon EffectsIn the liver, glucagon acts through a GPCR cAMP/PKA pathway to stimulate the production and release of glucose through activating gluconeogenesis and glycogenolysis. Glucagon also inhibits glycolysis and lipogenesis which has a glucose sparing effect. Glucagon stimulates fatty acid oxidation, which produces ATP to meet the energy demands of the cells. Finally, glucagon stimulates the uptake of amino acids by the liver, which are used as substrates for gluconeogenesis. Thus, glucagon converts the liver from an organ of glucose storage to an organ of glucose production. " "Glucagon EffectsIn the liver, glucagon acts through a GPCR [...] pathway to stimulate the production and release of glucose through activating gluconeogenesis and glycogenolysis. Glucagon also inhibits glycolysis and lipogenesis which has a glucose sparing effect. Glucagon stimulates fatty acid oxidation, which produces ATP to meet the energy demands of the cells. Finally, glucagon stimulates the uptake of amino acids by the liver, which are used as substrates for gluconeogenesis. Thus, glucagon converts the liver from an organ of glucose storage to an organ of glucose production." "Glucagon EffectsIn the liver, glucagon acts through a GPCR cAMP/PKA pathway to stimulate the production and release of glucose through activating gluconeogenesis and glycogenolysis. Glucagon also inhibits glycolysis and lipogenesis which has a glucose sparing effect. Glucagon stimulates fatty acid oxidation, which produces ATP to meet the energy demands of the cells. Finally, glucagon stimulates the uptake of amino acids by the liver, which are used as substrates for gluconeogenesis. Thus, glucagon converts the liver from an organ of glucose storage to an organ of glucose production. " "Glucagon EffectsIn the liver, glucagon stimulates gluconeogenesis by stimulating the production of phosphoenolpyruvate carboxykinase (PEPCK), and fructose 1,6 bisphosphatase (FBPase) and [...]. Glycogenolysis is stimulated by activating glycogen phosphorylase and suppressing glycogen synthase." "Glucagon EffectsIn the liver, glucagon stimulates gluconeogenesis by stimulating the production of phosphoenolpyruvate carboxykinase (PEPCK), and fructose 1,6 bisphosphatase (FBPase) and glucose-6-phosphatase (G6Pase). Glycogenolysis is stimulated by activating glycogen phosphorylase and suppressing glycogen synthase. " "Glucagon EffectsIn the liver, glucagon stimulates gluconeogenesis by stimulating the production of [...], and [...] and glucose-6-phosphatase (G6Pase). Glycogenolysis is stimulated by activating glycogen phosphorylase and suppressing glycogen synthase." "Glucagon EffectsIn the liver, glucagon stimulates gluconeogenesis by stimulating the production of phosphoenolpyruvate carboxykinase (PEPCK), and fructose 1,6 bisphosphatase (FBPase) and glucose-6-phosphatase (G6Pase). Glycogenolysis is stimulated by activating glycogen phosphorylase and suppressing glycogen synthase. " "Glucagon EffectsIn the liver, glucagon stimulates gluconeogenesis by stimulating the production of phosphoenolpyruvate carboxykinase (PEPCK), and fructose 1,6 bisphosphatase (FBPase) and glucose-6-phosphatase (G6Pase). Glycogenolysis is stimulated by activating [...] and suppressing [...]." "Glucagon EffectsIn the liver, glucagon stimulates gluconeogenesis by stimulating the production of phosphoenolpyruvate carboxykinase (PEPCK), and fructose 1,6 bisphosphatase (FBPase) and glucose-6-phosphatase (G6Pase). Glycogenolysis is stimulated by activating glycogen phosphorylase and suppressing glycogen synthase. " "Glucagon EffectsBecause glucose shifts [...] towards gluconeogenesis, the nitrogen lost by the [...] is converted to urea and excreted, tending to cause negative nitrogen balance, while the stimulation of lipolysis in the adipose tissue increases the flux of fatty acids to the liver, providing substrate for an increased production of ketone bodies. Hyperglycemia, negative nitrogen balance and ketosis are hallmarks of diabetes mellitus. Excessive secretion of glucagon has been demonstrated in diabetes, compounding the difficulties created by insulin insufficiency." "Glucagon EffectsBecause glucose shifts amino acids towards gluconeogenesis, the nitrogen lost by the amino acids is converted to urea and excreted, tending to cause negative nitrogen balance, while the stimulation of lipolysis in the adipose tissue increases the flux of fatty acids to the liver, providing substrate for an increased production of ketone bodies. Hyperglycemia, negative nitrogen balance and ketosis are hallmarks of diabetes mellitus. Excessive secretion of glucagon has been demonstrated in diabetes, compounding the difficulties created by insulin insufficiency. " "Glucagon EffectsBecause glucose shifts amino acids towards gluconeogenesis, the nitrogen lost by the amino acids is converted to urea and excreted, tending to cause negative nitrogen balance, while the stimulation of lipolysis in the adipose tissue increases the flux of fatty acids to the liver, providing substrate for an increased production of ketone bodies. [...], negative nitrogen balance and ketosis are hallmarks of diabetes mellitus. Excessive secretion of [...] has been demonstrated in diabetes, compounding the difficulties created by insulin insufficiency." "Glucagon EffectsBecause glucose shifts amino acids towards gluconeogenesis, the nitrogen lost by the amino acids is converted to urea and excreted, tending to cause negative nitrogen balance, while the stimulation of lipolysis in the adipose tissue increases the flux of fatty acids to the liver, providing substrate for an increased production of ketone bodies. Hyperglycemia, negative nitrogen balance and ketosis are hallmarks of diabetes mellitus. Excessive secretion of glucagon has been demonstrated in diabetes, compounding the difficulties created by insulin insufficiency. " "Glucagon EffectsBecause glucose shifts amino acids towards gluconeogenesis, the nitrogen lost by the amino acids is converted to urea and excreted, tending to cause [...] nitrogen balance, while the stimulation of lipolysis in the adipose tissue increases the flux of fatty acids to the liver, providing substrate for an increased production of [...]. Hyperglycemia, [...] nitrogen balance and [...] are hallmarks of diabetes mellitus. Excessive secretion of glucagon has been demonstrated in diabetes, compounding the difficulties created by insulin insufficiency." "Glucagon EffectsBecause glucose shifts amino acids towards gluconeogenesis, the nitrogen lost by the amino acids is converted to urea and excreted, tending to cause negative nitrogen balance, while the stimulation of lipolysis in the adipose tissue increases the flux of fatty acids to the liver, providing substrate for an increased production of ketone bodies. Hyperglycemia, negative nitrogen balance and ketosis are hallmarks of diabetes mellitus. Excessive secretion of glucagon has been demonstrated in diabetes, compounding the difficulties created by insulin insufficiency. " "Glucagon Regulation[...] stimulate both insulin and glucagon secretion. This concurrent stimulation of both glucagon and insulin secretion occurs after a [...] meal is consumed. Glucagon acts to stimulate diversion of excess amino acids, which cannot be stored, into glucose via gluconeogensis in the liver. This prevents the hypoglycemia that could result from a pure protein diet but will also eventually lead to elevated plasma glucose. The amino acids stimulate insulin secretion at the same time to promote the absorption and storage of this glucose by muscle and fat tissue, thus preventing hyperglycemia." "Glucagon RegulationAmino acids stimulate both insulin and glucagon secretion. This concurrent stimulation of both glucagon and insulin secretion occurs after a pure protein meal is consumed. Glucagon acts to stimulate diversion of excess amino acids, which cannot be stored, into glucose via gluconeogensis in the liver. This prevents the hypoglycemia that could result from a pure protein diet but will also eventually lead to elevated plasma glucose. The amino acids stimulate insulin secretion at the same time to promote the absorption and storage of this glucose by muscle and fat tissue, thus preventing hyperglycemia. " "Glucagon RegulationAmino acids stimulate both insulin and glucagon secretion. This concurrent stimulation of both glucagon and insulin secretion occurs after a pure protein meal is consumed. Glucagon acts to stimulate diversion of excess amino acids, which cannot be stored, into glucose via gluconeogensis in the liver. This prevents the hypoglycemia that could result from a pure protein diet but will also eventually lead to elevated plasma glucose. The amino acids stimulate insulin secretion at the same time to promote the [...] and [...] of this glucose by muscle and fat tissue, thus preventing [...]." "Glucagon RegulationAmino acids stimulate both insulin and glucagon secretion. This concurrent stimulation of both glucagon and insulin secretion occurs after a pure protein meal is consumed. Glucagon acts to stimulate diversion of excess amino acids, which cannot be stored, into glucose via gluconeogensis in the liver. This prevents the hypoglycemia that could result from a pure protein diet but will also eventually lead to elevated plasma glucose. The amino acids stimulate insulin secretion at the same time to promote the absorption and storage of this glucose by muscle and fat tissue, thus preventing hyperglycemia. " "Glucagon RegulationAmino acids stimulate both insulin and glucagon secretion. This concurrent stimulation of both glucagon and insulin secretion occurs after a pure protein meal is consumed. Glucagon acts to stimulate diversion of excess amino acids, which cannot be stored, into glucose via [...] in the liver. This prevents the [...] that could result from a pure protein diet but will also eventually lead to elevated plasma glucose. The amino acids stimulate insulin secretion at the same time to promote the absorption and storage of this glucose by muscle and fat tissue, thus preventing hyperglycemia." "Glucagon RegulationAmino acids stimulate both insulin and glucagon secretion. This concurrent stimulation of both glucagon and insulin secretion occurs after a pure protein meal is consumed. Glucagon acts to stimulate diversion of excess amino acids, which cannot be stored, into glucose via gluconeogensis in the liver. This prevents the hypoglycemia that could result from a pure protein diet but will also eventually lead to elevated plasma glucose. The amino acids stimulate insulin secretion at the same time to promote the absorption and storage of this glucose by muscle and fat tissue, thus preventing hyperglycemia. " "Endocrine Pancreas PathologiesType 1 diabetes is caused by autoimmune destruction of beta islet cells. Possible treatments include [...], [...], immuno-modulation treatments, and tissue regeneration from stem cells. " "Endocrine Pancreas PathologiesType 1 diabetes is caused by autoimmune destruction of beta islet cells. Possible treatments include hormone replacement, organ transplant, immuno-modulation treatments, and tissue regeneration from stem cells.  " "Endocrine Pancreas Pathologies[...] is caused by autoimmune destruction of [...] islet cells. Possible treatments include hormone replacement, organ transplant, immuno-modulation treatments, and tissue regeneration from stem cells. " "Endocrine Pancreas PathologiesType 1 diabetes is caused by autoimmune destruction of beta islet cells. Possible treatments include hormone replacement, organ transplant, immuno-modulation treatments, and tissue regeneration from stem cells.  " "Endocrine Pancreas PathologiesType 2 diabetes has a more complex progression and is more difficult to treat. It involves development of [...] and [...], and can ultimately result in pancreatic failure. " "Endocrine Pancreas PathologiesType 2 diabetes has a more complex progression and is more difficult to treat. It involves development of insulin resistance and glucose intolerance, and can ultimately result in pancreatic failure.  " "Endocrine Pancreas Pathologies[...] has a more complex progression and is more difficult to treat. It involves development of insulin resistance and glucose intolerance, and can ultimately result in [...] failure. " "Endocrine Pancreas PathologiesType 2 diabetes has a more complex progression and is more difficult to treat. It involves development of insulin resistance and glucose intolerance, and can ultimately result in pancreatic failure.  "