Adrenaline adipose tissue

Hormones can modify the concentration of precursors, particularly the lipolytic hormones (growth hormone, glucagon, adrenaline) and cortisol. The lipolytic hormones stimulate lipolysis in adipose tissue so that they increase glycerol release and the glycerol is then available for gluconeogenesis. Cortisol increases protein degradation in muscle, which increases the release of amino acids (especially glutamine and alanine) from muscle (Chapter 18). 

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. 

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. 

Inhibition of adrenaline-stimulated lipolysis in adipose tissue. 

The mobilization of the depot fat of adipose tissues requires hydrolysis of the triglycerides. Adrenalin or other lipolytic hormones trigger a... 

Adrenalin (epinephrin) stimulates phosphorylation and inactivation in adipose tissue. 

The combination of norephedrine with caffeine works synergistically to drastically increase the body s production of adrenaline and noradrenaline-the primary adrenergic hormones. These hormones bind to the various adrenergic receptors, of which there are the beta sub 2, beta sub 3, and alpha sub 2 receptors, that together affect fat loss and fat dispersal. The stimulation of the beta sub 2 and the beta sub 3 receptors in particular is what s responsible for the mobilization and burning of adipose tissue (fat). These are the receptors that you want to stimulate to affect fat loss in a positive way and thankfully the caffeine/norephedrine combination is quite efficient at this. 

The catecholamines epinephrine and norepinephrine (adrenaline and noradrenaline) originate in the inner medullar region of the adrenal glands. Stimulation of the adrenal by the sympathetic nervous system leads to secretion of catecholamines into the bloodstream. In addition, adipose tissue is itself directly innervated by the sympathetic nervous system. Various types of metabolic stress trigger the sympathetic nervous system to release its neurotransmitter, norepinephrine, directly into adipose where its effects on the adipocyte are mediated by specific plasma membrane adrenoreceptors. Rapid reflex responses are primarily stimulated by the sympathetic nervous system, whereas more long-term (i.e., on the scale of hours, days, and weeks) and/or basal effects are subject to regulation by catecholamine secretion. 

In Topic 41, we considered in general terms the way in which hormones act as chemical messengers, transmitting information from one tissue to another. In this topic, we are going to look at three of the most important hormones and the way in which they control how we handle major foodstuffs in three major tissues muscle, liver and adipose tissue (which, between them, make up a high percentage of total body mass). The three hormones are insulin, glucagon and adrenaline, two of them produced by the pancreas and the third, as its name implies, by the adrenal medulla. Their effects, explained below, are summarised in Table 43.1. 

Activity Like the chemically and physiologically related (R)- noradrenaline (/f)-A., as an adrenal hormone, increases the degradation of glycogen in the liver and of fat in adipose tissue as well as the oxidative metabolism in muscle. As neutrotransmitter of the adrenergic nerve system (R)-A. increases heart rate as a sympathicomimetic, constricts blood vessels of the skin, mucous membranes, and abdominal viscera, and dilates vessels of the skeletal musculature and liver. The relaxation of smooth musculature in the intestine or bronchi effected by (R)-A. leads to a reduction of peristalsis (intestinal movements) or to dilatation of the bronchi. (S)-A. is about 12 times less active than (R)-adrenaline. 

Herrera and Renold (1960) have observed that cortisol in vitro decreases the recovciy of C from glycine-i-C in the trichloroacetic acid-precipitable protein of epididymal adipose tissue (sec Section IV, H). Interest in this observation centers on the possibility that it may reflect the well-known effects of the glucocorticoids on protein metabolism. It has also been noted that cortisol in vitro decreases the glucose uptake of epididymal adipose tissue incubated in the presence of adrenaline, ACTH, or growth hormone (Renold et al., 1960b). 

Ohminami, H., Y. Kimura, H. Okuda, T. Tani, S. Arichi, and T. Hayashi Effects of Ginseng Saponins on the Actions of Adrenalin, ACTH and Insulin on Lipolysis and Lipogenesis in Adipose Tissue. Planta Medica 41, 351 (1981). 

Hormone-sensitive lipase tissue activity is stimulated by adrenaline (epinephrine), glucagon, ACTH (corticotropin), TSH (thyrotropin) and serotonin (Jensen, 1971). These hormones are presumed to exert their effects on adipose tissue by stimulating adenylate cyclase. Certainly, an increased formation of cAMP (cyclic AMP) is brought about by lipolytic hormones and cAMP has been shown to stimulate lipase activity in cell-free preparations (cf. O Doherty, 1978). 

During fasting or starvation, the catabohc hormones glucagon and cortisol are secreted from the a-ceUs of the pancreas and the adrenal cortex, respectively. In response to severe stress or danger, adrenaline is secreted by the adrenal medulla. These hormones stimulate hormone-sensitive lipase that mobilises fatty acids and glycerol from white adipose tissue. 

---