Peripheral Endocrine Glands 1 PDF
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Goldsmith
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Summary
This document provides a detailed overview of peripheral endocrine glands, including the endocrine control of fuel and calcium metabolism, adrenal glands, and the thyroid gland. The document also discusses fuel metabolism, including anabolism, catabolism, and the role of digestion in the process. Various aspects of nutrient storage (glucose, fat acids, and amino acids) are also explored.
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The Peripheral Endocrine Glands 1 Goldsmith ⚫ Endocrine control of fuel metabolism ⚫ Endocrine control of calcium metabolism ⚫ Adrenal glands ⚫ Thyroid gland Peripheral endocrine glands ⚫ Endocrine pancreas: important in metabolizing nutrients ⚫...
The Peripheral Endocrine Glands 1 Goldsmith ⚫ Endocrine control of fuel metabolism ⚫ Endocrine control of calcium metabolism ⚫ Adrenal glands ⚫ Thyroid gland Peripheral endocrine glands ⚫ Endocrine pancreas: important in metabolizing nutrients ⚫ Parathyroid glands: important for Ca2+ metabolism ⚫ Adrenal glands: important for metabolizing nutrients, adapting to stress, maintaining salt balance ⚫ Thyroid: controls body’s basal metabolic rate 1 Objectives ⚫ After completion of this section, you will be able to: ⚫ describe the basics of nutrient metabolism ⚫ explain the central role of glucose in metabolism ⚫ explain the means by which nutrients are stored ⚫ define basic terms associated with nutrient metabolism ⚫ describe the pancreas’ role in nutrient metabolism ⚫ Describe the major cells of the endocrine pancreas and their secretions ⚫ Explain the effects of insulin and glucagon ⚫ Explain the synthesis of, control of production, and feedback for insulin and glucagon Fuel metabolism ⚫ Metabolism: all of the chemical reactions within the cells of the body ⚫ Fuel metabolism (AKA, intermediary metabolism): degradation, synthesis, and transformation of proteins, carbohydrates, and lipids ⚫ Digestion: macromolecules broken down into smaller absorbable subunits 2 Fuel metabolism (cont.) ⚫ Anabolism: synthesis of large organic molecules ⚫ Anabolic reactions require ATP ⚫ Catabolism: breakdown of large molecules ⚫ Reactions (hydrolysis and oxidation) make ATP ⚫ Smaller subunits produced by catabolism can be used for energy or cellular synthesis 3 Nutrient storage: glucose ⚫ Nutrients from meals must be stored and released between meals ⚫ Excess circulating glucose: stored as glycogen in the liver and skeletal muscles ⚫ Glycogen storage is limited ⚫ Once reach limit, rest is stored as triglycerides in adipose tissue Nutrient storage: glucose ⚫ The brain needs a constant supply of glucose ⚫ Cannot store glycogen ⚫ Thus, blood glucose concentration highly regulated ⚫ Fasting: many body cells burn fatty acids to spare glucose for the brain ⚫ To supply the brain, amino acids can be converted to glucose by gluconeogenesis 4 Nutrient storage: fat acids and amino acids ⚫ Excess circulating fatty acids: incorporated into triglycerides, mainly in adipose tissue ⚫ Excess amino acids: converted to glucose and fatty acids; ultimately stored as triglycerides in adipose tissue ⚫ Muscles are the main site of amino acid storage via structural proteins ⚫ Proteins are not first choice for E, though, as they serve essential functions Nutrient storage and use ⚫ Two functional metabolic states: ⚫ Absorptive (fed) state: occurs when ingested nutrients are being absorbed into the blood following a meal (~ 4 hours) ⚫ Metabolic fuels are stored during the absorptive state ⚫ Postabsorptive (fasting) state: Nutrients are not being absorbed at this time (between meals) ⚫ Metabolic fuels are mobilized during the postabsorptive state ⚫ Stored molecules are catabolized to maintain glucose concentration and for E production 5 6 Fuel metabolism regulation ⚫ Insulin and glucagon from pancreas regulate fuel metabolism ⚫ Pancreas: Endocrine cells in pancreas organized into the islets of Langerhans ⚫ b cells produce insulin ⚫ a cells produce glucagon ⚫ Somatostatin from pancreatic D cells can inhibit both ⚫ Epsilon cells: ghrelin ⚫ Gamma, or F cells: pancreatic polypeptide 7 Insulin: effects ⚫ Lowers blood glucose, fatty acid, and amino acid levels; promotes their storage ⚫ Facilitates glucose transport into most cells ⚫ Glucose transporters (GLUTs) act as plasma membrane carriers to accomplish this process: ONLY GLUT-4 is insulin responsive (skeletal muscle during rest and adipose cells) ⚫ Insulin and this transporter also assist the transport of fatty acids into tissues ⚫ Stimulates glycogenesis in skeletal muscle and liver cells ⚫ Inhibits glycogenolysis and gluconeogenesis ⚫ Catalyzes the production of fatty acids from glucose ⚫ Promotes entry of fatty acids from blood into adipose ⚫ Promotes the transport and incorporation of amino acids into cells for protein synthesis Insulin stimulation ⚫ Increase in blood glucose concentration (e.g., during absorptive state) increases insulin secretion* ⚫ This brings blood glucose down to a normal level ⚫ Decrease in glucose below normal inhibits insulin secretion ⚫ This shifts metabolism from the absorptive to the postabsorptive state ⚫ Elevated blood amino acids stimulate insulin secretion ⚫ Gastrointestinal hormones stimulate insulin secretion ⚫ Parasympathetic nervous system increases insulin secretion (sympathetic decreases) ⚫ Inadequate insulin action produces diabetes mellitus, resulting in hyperglycemia ⚫ Type I diabetes mellitus: due to insulin deficiency ⚫ Type II: due to reduced sensitivity of target cells to insulin 8 Insulin secretion 9 Glucagon ⚫ Opposes the actions of insulin ⚫ Promotes glycogenolysis and stimulates gluconeogenesis ⚫ Promotes fat breakdown ⚫ Promotes protein breakdown in the liver ⚫ Glucagon secretion increases during the postabsorptive state ⚫ Secretion increases when blood glucose concentration is too low Glucagon (cont.) ⚫ No known abnormalities due to glucagon deficiency ⚫ However, excess glucagon can aggravate the hyperglycemia of diabetes mellitus ⚫ Growth hormone, cortisol, epinephrine, and glucagon are insulin antagonists ⚫ That is, they increase blood glucose ⚫ Insulin and glucagon work as a team to control blood concentration of glucose and fatty acids 10 11