Adipose tissue hormones secreted

In Type I diabetes mellitus, there is a severe deficiency (or total absence) of insulin due to an autoimmune attack on the cells that produce insulin, pancreatic j8-cells. The absence of insulin produces a deficiency in adipose tissue lipoprotein lipase. This causes sluggish catabolism of VLDL and leads to hypertriglyceridemia. Another mechanism by which insulin deficiency promotes increased VLDL levels is the failure to inhibit the activity of adipose tissue hormone-sensitive lipase. This enzyme hydrolyzes cytoplasmic triglyceride droplets. The fatty acids then go to the liver, where they are re-esterified to form triglycerides. These triglycerides are exported on VLDL particles. Since adipose tissue-derived fatty acids are an important substrate for hepatic VLDL triglycerides, the failure to suppress adipose tissue lipolysis is an important contributor to the enhanced rate of VLDL triglyceride secretion. 

The hypertriglyceridemia of Type II diabetes, unlike that which is found with Type I diabetes, is not due to excessive adipocyte lipolysis. This is because only a small level of insulin action is required to suppress excessive adipose tissue hormone-sensitive lipase activity. In Type II diabetes, there is insufficient adipose tissue lipoprotein lipase and excessive hepatic triglyceride synthesis. Thus, inefficient VLDL triglyceride catabolism and excessive VLDL triglyceride secretion both contribute to the excess VLDL in Type II diabetes. 

Insulin is a peptide hormone, secreted by the pancreas, that regulates glucose metabolism in the body. Insufficient production of insulin or failure of insulin to stimulate target sites in liver, muscle, and adipose tissue leads to the serious metabolic disorder known as diabetes mellitus. Diabetes afflicts millions of people worldwide. Diabetic individuals typically exhibit high levels of glucose in the blood, but insulin injection therapy allows diabetic individuals to maintain normal levels of blood glucose. 

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. 

In addition to fiber and carbohydrate content, protein intake from legumes may have weight-loss benefits for obese individuals just because proteins enhance post-meal satiety (Rolls, 1995). However, a possible specific role for phytoestrogens in obesity has been postulated through the modulation of the satiety response, a neuroendocrine mechanism controlled by leptin (a hormone secreted by adipose tissue and already known to be regulated by... 

Many of the endocrine glands are listed in Table 4.1. This table includes not only the well-accepted hormone-secreting tissues but also those such as adipose tissue (see Chapter 9 for further details), which also have secretory activities. 

Other hormones Thyroxine has long been known to increase metabolic rate, although the mechanism for this effect is not totally clear (Silvestri et al. 2005). More recently the hormone leptin, which is secreted by adipose tissue, has also been found to increase the metabolic rate. This effect of leptin is considered to play a role in controlling the amount of adipose tissue in the body, although this is a controversial subject (Chapter 12). 

In the ebb phase, there is increased activity of the sympathetic nervous system and increased plasma levels of adrenaline and glucocorticoids but a decreased level of insulin. This results in mobilisation of glycogen in the liver and triacylglycerol in adipose tissue, so that the levels of two major fuels in the blood, glucose and long-chain fatty acids, are increased. This is, effectively, the stress response to trauma. These changes continue and are extended into the flow phase as the immune cells are activated and secrete the proinflammatory cytokines that further stimulate the mobilisation of fuel stores (Table 18.2). Thus the sequence is trauma increased endocrine hormone levels increased immune response increased levels of cytokines metabolic responses. 

The endocrine pancreas responds to this by altering its hormone release—there is an increase in insulin secretion and a reduction in glucagon secretion. The increase in the insu-lin/glucagon quotient and the availability of substrates trigger an anabolic phase in the tissues—particularly liver, muscle, and adipose tissues. 

CM and VLDL secreted by intestinal cells and VLDL synthesized and secreted in the liver have similar metabolic fates. After secretion into the blood, newly formed CM and VLDL take up apoprotein (apo-C) from HDL and are subsequently removed from the blood (plasma half-life of less than 1 h in humans [137]) primarily by the action of lipoprotein lipase (LPL). Lipoprotein lipase is situated mainly in the vascular bed of the heart, skeletal muscle, and adipose tissue and catalyzes the breakdown of core TG to monoglycerides and free fatty acids, which are taken up into adjacent cells or recirculated in blood bound to albumin. The activity of LPL in the heart and skeletal muscle is inversely correlated with its activity in adipose tissue and is regulated by various hormones. Thus, in the fasted state, TG in CM and VLDL is preferentially delivered to the heart and skeletal muscle under the influence of adrenaline and glucagon, whereas in the fed state, insulin enhances LPL activity in adipose tissue, resulting in preferential uptake of TG into adipose tissue for storage as fat. 

ACTH (adrenocorticotropic hormone, corticotropin) is a 39-amino-acid peptide synthesized and secreted by the corticotrope cells of the anterior lobe of the pituitary gland. ACTH acts on several target tissues, including the adrenal cortex, adipose tissue and brain. It is synthesized as part of proopiomelanocortin (POMC) as amino acids 132-170 of this molecule, which is proteolytically cleaved to produce ACTH [1],... 

Peripheral tissues such as muscle, adipose tissue, and the lactating breast contain both hormone-sensitive lipase and lipoprotein lipase. This second lipase, mentioned in the lipoprotein section of Chapter 6, requires apolipoprotein C-II as a cofactor. The lipase is secreted by cells and migrates through the interstitial fluid to the capillary, where it becomes bound to the membrane with its active site exposed to the bloodstream. This binding to the luminal wall of the capillary occurs by attachment to a polymer called glycosaminoglycan. 

---