Physiology Lecture 23 PDF

Physiology Lecture 23 What are the three forms of energy storage in the body? The three forms of energy storage are glycogen, triglycerides, and protein. Where is glycogen stored, and how long does it last? Glycogen is stored in th...

Physiology Lecture 23 What are the three forms of energy storage in the body? The three forms of energy storage are glycogen, triglycerides, and protein. Where is glycogen stored, and how long does it last? Glycogen is stored in the liver and muscle, with a small reservoir lasting less than one day. Only the liver can supply glycogen to other tissues. Where are triglycerides stored, and how long can they provide energy? Triglycerides are stored in adipose tissue and represent the largest energy reservoir, lasting several weeks. Where is protein stored, and why is its use for energy considered costly? Protein is stored in muscle, forming a large energy reservoir. However, its use for energy is considered costly because it involves breaking down functional muscle tissue. What happens to glucose during the digestive phase? During the digestive phase, glucose is taken into skeletal muscle, liver, and adipose tissue. How is glucose stored in the body during the digestive phase? Glucose is stored as glycogen and/or triglycerides (TG). What is the source of glucose, amino acids, and FFA during the fasting phase? glucose is derived from the liver. Amino acids are obtained from skeletal muscle Free fatty acids are released from adipose tissue Which hormone primarily controls anabolic processes for nutrient metabolism? Insulin primarily controls anabolic processes, with increased levels promoting nutrient storage. Which hormones are counter-regulatory and promote catabolism? Physiology Lecture 23 1  glucagon epinephrine, growth hormone (GH), cortisol. (An exception is protein anabolism, which involves IGF-1.) TH what is the dominant regulator insulin glucagon releases glucose from storage Acts almost exclusively on liver Epinephrine Epinephrine is a hormone important in exercise and stress. It acts on muscle and adipose tissue, stimulating glycogenolysis to provide glucose and lipolysis to release fatty acids for energy. Epinephrine also increases cardiac output and improves blood delivery to muscles and vital organs, enhancing oxygen and nutrient transport Growth hormone role in energy? increases lean body mass by promoting protein anabolism in muscles and mobilizes energy through its carbohydrate and lipid catabolic effects. It reduces insulin sensitivity in peripheral tissues, leading to higher blood glucose levels. Prolonged GH exposure can stimulate glucose production in the kidneys and plays a role in regulating acidosis and ammonia (NH3) production during metabolic stress. Cortisol (glucocorticoids) role in energy? Cortisol is essential for life and energy regulation. It has permissive effects with hormones like glucagon and epinephrine, enabling them to act effectively. Physiology Lecture 23 2  It stimulates hepatic gluconeogenesis to maintain blood glucose levels promotes protein catabolism to provide amino acids for energy, and supports lipid metabolism. These actions ensure the body has energy during stress or fasting. Thyroid hormone role in energy? Main effect is a permissive one cortisol effect with other hormones on sugar levels Physiology Lecture 23 3  What happens to metabolism during exercise? During exercise, plasma glucose remains steady as the liver releases glucose to match increased skeletal muscle uptake. Insulin levels fall, reducing storage processes and promoting the release of glucose and fats for energy. Physiology Lecture 23 4  How does the body meet energy needs during exercise? The body adapts to meet energy demands during exercise by regulating energy expenditure and mobilizing different fuel sources. Fat oxidation cannot sustain higher-intensity activities, which rely on glycogen. Glucose intake during exercise must be controlled to avoid disrupting free fatty acid availability or misdirecting glucose to non-working tissues. Muscle fatigue is closely linked to glycogen depletion, though it is not the sole cause. Carbo-loading increases glycogen stores to delay fatigue but does not guarantee improved performance. Physiology Lecture 23 5  alpha and beta cells α-cell -- Glucagon ß-cell -- Insulin somatostatin inhibit glucagon and insulin C peptide is useful for diagnostic purposes of endogenous insulin production Insulin Secretionontrolled by nutrients, hormons and nerve Closure of ATP- dependent K+-channel by ß-cell glucose metabolism Physiology Lecture 23 6  Glucose enters pancreatic β-cells via GLUT2 transporters and undergoes metabolism, increasing ATP levels. The rise in ATP closes ATP-sensitive K+channels, causing membrane depolarization. This opens voltage-gated calcium channels, leading to calcium influx, which triggers insulin secretion. additional control of insulin secretion GLP1 Amino Acid Epinephrine and norepinephrine (inhibit) oral administration are more efficient than intravenous for insulin response In vivo Secretion -- Biphasic Biphasic insulin secretion consists of two phases: the initial burst and the secondary phase. The initial burst occurs rapidly and represents the release of pre-formed insulin stored in secretory granules. The secondary phase is slower and involves the synthesis of new insulin, followed by its secretion. α-adrenergic receptor activity inhibit insulin Physiology Lecture 23 7  Actions of Insulin Acute effects on Skeletal Muscle Insulin Independent glucose transport with muscle activity qirh glut 4 Actions of Insulin Acute effects on Liver Insulin Independent glucose transport into liver with GLUT-2 decreases ketogenesis Actions of Insulin Acute effects on Adipose Tissue Insulin Independent glucose transport with muscle activity with glut 4 Increased FFA storage Increased activity of Lipoprotein Lipase (LPL) Decreased activity of Hormone Sensitive Lipase (HSL) Decreased Insulin ➔ Increased Lipolysis long term effect of Prolonged Insulin Deficiency glucagon main target Physiology Lecture 23 8  liver FFA indirectly increase Glucose synthesis FFA cannot be directly converted to glucose FFA release also acts as a “glucose sparing” effect. Glucagon Lipid/Protein Actions Increase in plasma ketones Requires presence of increased plasma FFA GLP1 and glucagon inhibit what happens during and after sprint, during marathon, after marathon during sprint, too quick for hormonal activity after sprint, repletion from liver to muscle during marathon nearly all metabolic hormones are active after marathon, repletion by eating Physiology Lecture 23 9