Liver blood glucose level

The first hormonal signal found to comply with the characteristics of both a satiety and an adiposity signal was insulin [1]. Insulin levels reflect substrate (carbohydrate) intake and stores, as they rise with blood glucose levels and fall with starvation. In addition, they may reflect the size of adipose stores, because a fatter person secretes more insulin than a lean individual in response to a given increase of blood glucose. This increased insulin secretion in obesity can be explained by the reduced insulin sensitivity of liver, muscle, and adipose tissue. Insulin is known to enter the brain, and direct administration of insulin to the brain reduces food intake. The adipostatic role of insulin is supported by the observation that mutant mice lacking the neuronal insulin receptor (NDRKO mice) develop obesity. 

Insulin resistance occurs when the normal response to a given amount of insulin is reduced. Resistance of liver to the effects of insulin results in inadequate suppression of hepatic glucose production insulin resistance of skeletal muscle reduces the amount of glucose taken out of the circulation into skeletal muscle for storage and insulin resistance of adipose tissue results in impaired suppression of lipolysis and increased levels of free fatty acids. Therefore, insulin resistance is associated with a cluster of metabolic abnormalities including elevated blood glucose levels, abnormal blood lipid profile (dyslipidemia), hypertension, and increased expression of inflammatory markers (inflammation). Insulin resistance and this cluster of metabolic abnormalities is strongly associated with obesity, predominantly abdominal (visceral) obesity, and physical inactivity and increased risk for type 2 diabetes, cardiovascular and renal disease, as well as some forms of cancer. In addition to obesity, other situations in which insulin resistance occurs includes... 

Insulin is a hormone manufactured by the beta cells of the pancreas. It is the principal hormone required for the proper use of glucose (carbohydrate) by the body. Insulin also controls the storage and utilization of amino acids and fatty acids. Insulin lowers blood glucose levels by inhibiting glucose production by the liver. 

The liver maintains blood glucose levels, makes fat, makes ketone bodies, and stores glycogen. 

A major function of hGH is the promotion of anabolic activity, that is, bone and tissue growth due to increase in metabolic processes. Other biological effects of hGH are stimulation of protein synthesis, elevation of blood glucose level, and improvement of liver function. 

It is possible that, via a cycle, the direction of a flux can be completely reversed. An example is glucose metabolism in the liver at a low blood glucose level the hver releases glucose, whereas at a high concentration of blood glucose the liver takes up glucose. This is the result of a... 

The function of glucagon is to respond rapidly to an acute fall in the blood glucose level by stimulating glucose release by the liver and fatty acid release by adipose tissue. 

Figure 12.18 Sites at which insulin stimulates glycogen synthesis in muscle. An increase in the blood glucose level, after a meal, increases secretion of insulin from the p-cells in the Islets of Langerhans. Insulin increases the transport of glucose into the muscle fibre and the activity of glycogen synthase (Chapter 6). The result is that insulin increases the rate of glycogen synthesis without marked changes in concentrations of glucose 6-phos-phate, glucose 1-phosphate or UDP-glucose in the liver.

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