Endocrine and Breast Module - Hyperglycemia Effects

A1C is a blood test that measures the average blood sugar level over the past 2-3 months.

A fasting blood glucose level of 7.0 mmol/L or higher on two separate occasions indicates diabetes.

Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs when the body produces excess ketones due to a lack of insulin.

Hyperglycemia is a condition where the blood sugar level is higher than normal.

Chronic hyperglycemia can lead to complications like cardiovascular disease, kidney disease, and nerve damage.

A hormone secreted by alpha cells in the pancreas that raises blood glucose levels by stimulating glycogen breakdown and gluconeogenesis.

A peptide hormone produced by L cells in the intestines that stimulates insulin secretion and promotes glucose homeostasis after meals.

A peptide hormone produced by L cells in the intestines that promotes intestinal growth and absorption.

The process by which hormones are released from cells into the bloodstream.

The state of low blood glucose levels.

The state of high blood glucose levels.

The process by which insulin secretion is stimulated by the presence of glucose in the bloodstream.

The process by which a cell's membrane potential changes due to the movement of ions across the membrane.

Glucagon release is triggered when blood glucose levels are low. It's like the body's "glucose alarm" that promotes glycogen breakdown and glucose synthesis to restore normal blood sugar.

Increased ATP levels in alpha cells due to high blood glucose inhibit glucagon release. The cell membrane stays polarized, closing calcium channels, preventing glucagon secretion.

Low blood glucose levels lead to low ATP levels in alpha cells. This keeps potassium channels open, causing membrane depolarization and opening calcium channels. This influx of calcium triggers glucagon secretion.

Low plasma fatty acids signal an energy deficit. Glucagon stimulates fat breakdown to restore energy balance. It's like using fat as a backup energy source.

High plasma amino acids, especially after protein-rich meals, stimulate both glucagon and insulin release to balance glucose levels.

Adrenaline increases glucagon secretion, preparing the body for energy demand by promoting glucose availability. Think of adrenaline as the "fight or flight" hormone.

High blood glucose directly inhibits glucagon release by signaling sufficient energy availability. This mechanism counteracts the stimulating effect of insulin.

Insulin, released from beta cells, inhibits glucagon release from neighboring alpha cells. This paracrine effect helps regulate blood glucose levels.

Glucagon is a peptide hormone that is produced by alpha cells in the pancreas. Its primary role is to increase blood glucose levels when they fall, acting as a counter-regulatory hormone to insulin. Glucagon's action is essential for maintaining blood glucose levels during fasting and during physical activity.

Glucagon is stimulated by low blood glucose levels, often seen during fasting or exercise. High amino acid levels, like those found after a protein-rich meal, also trigger glucagon release. Epinephrine, a stress hormone, enhances glucagon's release. On the other hand, high blood glucose and insulin levels inhibit glucagon release, as there is no need for additional glucose in the blood.

Glucagon plays a key role in maintaining blood glucose levels during fasting or periods of low glucose availability. It acts by stimulating the breakdown of stored glycogen (glycogenolysis) in the liver, releasing glucose into the bloodstream. Glucagon also promotes the synthesis of glucose from non-carbohydrate sources (gluconeogenesis) in the liver, further increasing blood glucose.

The synthesis of glucagon begins with the production of a precursor molecule called pre-proglucagon in the rough endoplasmic reticulum (ER) of alpha cells. This precursor undergoes proteolytic processing in the ER, resulting in proglucagon. The conversion of proglucagon to mature glucagon occurs in the Golgi apparatus through the action of an enzyme called prohormone convertase 2 (PC2). The mature hormone is then packaged into secretory vesicles and stored for release.

The body's response to hypoglycemia involves a complex interplay of hormones and mechanisms designed to restore blood glucose levels. The primary hormone involved in this response is glucagon, which is released from pancreatic alpha cells. Glucagon acts to increase blood sugar levels by stimulating the breakdown of glycogen in the liver and promoting the synthesis of glucose from non-carbohydrate sources.

Insulin-dependent hypoglycemia is typically caused by an overdose of insulin or by increased insulin sensitivity. Post-prandial hypoglycemia occurs after meals and is often associated with rapid fluctuations in blood glucose levels. Fasting hypoglycemia can occur after prolonged periods of fasting or in individuals with certain metabolic disorders. Alcohol-induced hypoglycemia can occur when alcohol consumption inhibits gluconeogenesis, the process by which the liver produces glucose from non-carbohydrate sources.

Hypoglycemia, or low blood glucose, manifests as a range of symptoms, most commonly: - Weakness and fatigue. - Confusion and disorientation. - Tremors and sweating. - Headache and dizziness. - Hunger and nausea. - Anxiety and irritability. - Rapid heartbeat. - Blurred vision. - Seizures. - Coma.

Gluconeogenesis is the process of creating new glucose from non-carbohydrate sources such as amino acids or lactate. It's crucial for maintaining blood sugar levels during fasting or prolonged exercise when glucose stores are depleted.

Glycolysis is the breakdown of glucose into pyruvate for energy production. It's inhibited by glucagon to prevent glucose depletion during fasting or exercise.

Glycogenesis is the process of storing glucose as glycogen in the liver and muscles. It's inhibited by glucagon to make glucose available for other tissues.

Lipolysis is the breakdown of fats (triglycerides) into fatty acids and glycerol. It's stimulated by glucagon to provide an alternative fuel source when glucose is scarce.

Ketogenesis is the production of ketone bodies from fatty acids. It's promoted by glucagon, providing an alternative energy source for the brain during prolonged fasting.

Glucagon receptor is a type of G-protein coupled receptor (GPCR) found on the surface of cells, primarily in the liver. When glucagon binds to this receptor, it initiates a signaling cascade that leads to glucose production.

Incretins are hormones secreted by the gut in response to food intake. They play a crucial role in regulating blood glucose levels by stimulating insulin release and suppressing glucagon release.

GLP-1 (Glucagon-like peptide-1) and GIP (Glucose-dependent insulinotropic peptide) are the two primary incretins. They are released by cells in the small intestine (L-cells for GLP-1, K-cells for GIP). GLP-1 increases insulin and inhibits glucagon release, while GIP mainly enhances insulin release.

Glucagon is released when blood glucose levels are low, typically during fasting or exercise. High amino acid levels (after a protein-rich meal) and adrenaline (stress hormone) also stimulate glucagon release. High blood glucose levels and insulin inhibit glucagon release.

Glucagon stimulates glycogenolysis (glycogen breakdown) in the liver, releasing glucose into the blood. It also activates gluconeogenesis, the synthesis of new glucose from other molecules.

Glucagon binds to its receptor on liver cells, initiating a signaling cascade that eventually activates key enzymes involved in glycogenolysis and gluconeogenesis.

The two main types of incretins are GLP-1 (Glucagon-like peptide-1) and GIP (Glucose-dependent insulinotropic peptide). They are released by different cells in the small intestine and work to stimulate insulin release and suppress glucagon release, ultimately lowering blood glucose levels.

Glucagon is released when blood glucose levels are low, preventing hypoglycemia by stimulating glycogen breakdown (glycogenolysis) and glucose synthesis (gluconeogenesis).

High blood glucose levels directly inhibit glucagon release, signaling sufficient energy availability.

Low blood glucose levels lead to low ATP levels in alpha cells, which opens calcium channels and triggers glucagon secretion.

Low plasma fatty acids indicate an energy deficit. Glucagon promotes fat breakdown to restore energy balance.

High plasma amino acids, especially after a protein-rich meal, stimulate glucagon release.

Adrenaline, the 'fight or flight' hormone, enhances glucagon secretion, preparing the body for energy demand by promoting glucose availability.

Somatostatin, released by delta cells, inhibits both glucagon and insulin secretion. This helps prolong nutrient absorption by slowing down hormone release.

High blood glucose levels lead to high ATP in alpha cells, which closes potassium channels. The membrane stays polarized, closing calcium channels and preventing glucagon secretion.

Glucagon release is triggered when low blood glucose levels lead to low ATP in alpha cells.

Glucagon is a key hormone in mobilizing energy stores during periods of low blood glucose. It stimulates the breakdown of stored glycogen (glycogenolysis) in the liver, releasing glucose into the bloodstream. Glucagon also promotes gluconeogenesis, the production of new glucose from non-carbohydrate sources, further increasing blood glucose levels. It also stimulates lipolysis (fat breakdown) to provide alternative energy sources.

Glucagon is a powerful hormone that plays a crucial role in maintaining blood glucose levels, especially during fasting, exercise, or when glucose demands are high. It works opposite to insulin to ensure the body has sufficient energy sources.