Anti-lipolysis

In detail, adipocytes from visceral adipose tissue are more resistant to insuhn-induced anti-lipolysis and re-esterification of NEFA than those from leg and non-visceral body fat both in vitro [503, 504] and in vivo [505]. Various functional differences in these ceUs have been identified at the level of the insuhn receptor and the post-receptor insulin signahng cascade [503, 504]. PDE3B involved in hpolysis regulation by insuhn (see above. Fig. 11.7) and protein tyrosine phosphatases de-phosphorylating fhe insuhn receptor, such as PTPlb, could be affected in differen-... 

As to be expected from a peptide that has been highly conserved during evolution, NPY has many effects, e.g. in the central and peripheral nervous system, in the cardiovascular, metabolic and reproductive system. Central effects include a potent stimulation of food intake and appetite control [2], anxiolytic effects, anti-seizure activity and various forms of neuroendocrine modulation. In the central and peripheral nervous system NPY receptors (mostly Y2 subtype) mediate prejunctional inhibition of neurotransmitter release. In the periphery NPY is a potent direct vasoconstrictor, and it potentiates vasoconstriction by other agents (mostly via Yi receptors) despite reductions of renal blood flow, NPY enhances diuresis and natriuresis. NPY can inhibit pancreatic insulin release and inhibit lipolysis in adipocytes. It also can regulate gut motility and gastrointestinal and renal epithelial secretion. 

The second way in which fats deteriorate is oxidative lipolysis. This is an entirely different process in which oxygen free radicals add across double bonds. Oxidative rancidity can be prevented or reduced by several different routes. One way is to ensure that no double bonds are present. Another is to use anti-oxidants that act as free radical traps. Exposure to oxygen and ultraviolet light should be avoided. Reducing the temperature has no effect since free radical processes have a zero activation energy. 

An anti-lipolytic signal is transduced by the otj-adrenergics, and the a,-adrenergics are involved in a separate pathway. In short, although lipolysis is the observed outcome of catecholamine stimulation, it is the steady-state result of competition between two opposing pathways triggered by the same signal. 

Skeletal growth in acromegaly cannot simply be explained by an anti-insulinic effect, stimulation of lipolysis, or stimulation of protein synthesis because cartilage formation requires that collagen (conversion of protein to hydroxyproline) and cartilage (synthesis of chondroitin sulfate) be formed. Acromegalic serum... 

In these experiments there was a poor correlation between the effects of insulin on cyclic AMP levels and lipolysis. When insulin had its most pronounced anti-lipolytic effects (i. e., in the presence of epinephrine alone) it did not appear to lower cyclic AMP, and when insulin lowered cyclic AMP (in tissue incubated with epinephrine and caffeine) it did not inhibit lipolysis. A small rise in the cyclic AMP level in adipose tissue (from about 1. 5 x 10 7 mmoles/g to 3. 5 x 10"7 mmoles/ g) is enough to stimulate lipolysis maximally and cyclic AMP... 

Potentiation of other human growth hormone-stimulated systems include (a) lipolysis from Isolated rat fat cells (23), and (b) partial prevention of insulin-induced hypoglycemia in normal fasted and alloxan-diabetic rats (21). The mechanism of potentiation of growth hormone by PPP(H) cannot be determined on the basis of the data now available. Competition between PPP(H) and HGH for anti-... 

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