Hepatic glycogenolysis

Metformin restrains hepatic glucose production principally by suppression of gluconeogenesis. The mechanisms involve potentiation of insulin action and decreased hepatic extraction of certain gluconeogenic substrates such as lactate. In addition, metformin reduces the rate of hepatic glycogenolysis and decreases the activity of hepatic glucose-6-phosphatase. Insulin-stimulated glucose uptake and glycogenesis by skeletal muscle is increased by metformin mainly by increased... 

Crude extracts of V. minor have shown a hypotensive effect in experimental animals (76) which is believed to be owing almost entirely to its vincamine content (77), and success has been claimed for clinical studies in middle Europe of purified alkaloid extracts (78). Besides this property, vincamine also has a curare-like property (79) and is known to induce strychnine-like convulsions in rabbits (80). The ability of vincamine to reduce blood sugar in an acute test in rats is apparently not because of the inhibition of hepatic glycogenolysis (81). The medicinal uses of V. minor have recently been reviewed (82). 

Autonomic outputs. Hypoglycaemia and hypothermia both lead to snstained sympathetic responses. Subjects feel hungry and eat if possible, bnt they refine their other actions to suit the circumstances. Hypoglycaemia requires hepatic glycogenolysis and glnconeogenesis, while hypothermia requires increased heat prodnction and a redistribntion of blood flow. Sympathetic activity is controlled by the hypothalamns, which instrncts the adrenal medulla to secrete adrenalin. This is a rather blunt control, and so localised sympathetic responses (such as blood flow regulation) are mediated by individnal nerves. Parasympathetic activity can also respond to the hypothalamus, which controls the nnclens of the solitary tract. 

Skin sweat, piio motor Male ejaculation Blood platelet aggregation Metabolic effect hyperkalaemla 1 Metabolic effects hypokalaemia (p ) hepatic glycogenolysis (p ) lipolysis (P. P )... 

GIP stimulates insulin secretion only in the presence of mild to moderate hyperglycaemia (Andersen et al., 1978 Wahl et al., 1992), but not in the presence of normal glucose concentrations. In addition to secretion of insulin, GIP augments insulin-dependent inhibition of hepatic glycogenolysis (Elahi et al., 1986 Hartman et al., 1986). It also activates adipose tissue lipoprotein lipase (Eckel et al., 1978) and has been shown to stimulate fatty acid synthesis de novo in rat adipose tissue (Oben et al., 1991). 

The increase in glucose uptake with increased intensity of exercise is matched by hepatic glucose production to the extent that arterial glucose concentrations are elevated by very intense exercise. Hepatic glycogenolysis probably is enhanced by a decrease in the level of insulin and by an increase in levels of glucagon and epinephrine. 

A direct stimulatory effect on hepatic glycogenolysis Pj) mediated by cAMP-dependent phosphorylation of phosphorylase. This effect is dependent on prior storage of glycogen in the liver therefore, both insulin and cortisol serve to condition the liver for this effect. 

Glucagon Pancreas Stimulates hepatic glycogenolysis and inhibits motility... 

The effect of epinephrine in the liver, therefore, enhances or is synergistic with the effects of glucagon. Epinephrine release during bouts of hypoglycemia or during exercise can stimulate hepatic glycogenolysis and inhibit glycogen synthesis very rapidly. 

The hormonal changes that direct the inaeased hepatic glycogenolysis, hepatic gluconeogenesis, and adipose tissue include a decrease in insulin and an increase in glucagon, epinephrine, and norepinephrine. Plasma levels of growth hormone, cortisol, and thyroid-stimulating hormone (TSH) also increase and may make a contribution to... 

Chemistry, mechanism, and effects Glucagon is the product of the A cells of the endocrine pancreas. Like insulin, glucagon is a peptide but unlike insulin, glucagon acts on G protein-coupled receptors. Activation of glucagon receptors, which are located in heart, smooth muscle, and liver, stimulates adenylyl cyclase and increases intracellular cAMP. This results in increases in the heart rate and the force of contraction, increased hepatic glycogenolysis and gluconeogenesis and relaxation of smooth muscle. The smooth muscle effect is particularly marked in the gut. 

Thyroid hormones regulate the turnover of carbohydrates, lipids, and proteins. They promote glucose absorption, hepatic and renal gluconeogenesis, hepatic glycogenolysis, and glucose utilization in muscle and adipose tissue (18). They increase de novo cholesterol synthesis but increase low-density lipoprotein degradation and cholesterol disposal even more, leading to a net decrease in total and in low-density lipoprotein cholesterol plasma levels (19). Thyroid hormones are anabolic when present at normal concentrations they then stimulate the expression of many key enzymes of metabolism. ... 

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