Hormonal Control of Glycogen-Metabolizing Enzymes in Liver

Hems, Douglas A.

doi:10.1042/bst0060033

Cited by 5 publications

(2 citation statements)

References 13 publications

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“…188 -238 The speed at which the enhanced incorporation of inorganic phosphate occurs suggests enhanced turnover of phosphatidylinositol. 188 Although this phenomenon may help to regulate membrane-transport processes, 239 nothing is known about the mechanism or the physiologic significance of these observations. Metabolism of 1,2-diacyl-sn-glycerol.…”

Section: Hormonal Regulation Of Fatty Acid Oxidation and Complex Lipimentioning

confidence: 98%

Short-term Hormonal Control of Hepatic Lipogenesis

et al. 1980

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L ipids are essential components of all living cells, functioning as an energy store and playing an important role in all biologic membranes. Triacylglycerols, the storage form and most abundant of the glycerolipids, represent a highly concentrated form of energy, yielding twice as many calories per gram as carbohydrate or protein. The phospholipids are amphipathic compounds which, along with cholesterol, are found in membranes where they interact to provide a polar-faced, hydrophobic continuum of critical importance for proper cell structure and function.A major function of lipogenesis is to store (as triacylglycerols) the chemical energy or foodstuffs ingested above the immediate requirements of an organism. Contrary to protein, which is not stored, and to carbohydrate, which can only be stored in limited quantities, the capacity to store triacylglycerols is almost unlimited. The ability to keep large amounts of triacylglycerols on board would not be useful, however, if it were not possible to quickly and efficiently stop diverting foodstuffs into triacylglycerol formation and to quickly and efficiently start utilizing these compounds to provide the energy necessary to synthesize ATP. For this reason, mechanisms have evolved which finely tune the synthesis and degradation of triacylglycerol to the ever changing demand for ATP. In contrast, phospholipid and cholesterol synthesis must be, at least, partially maintained (or their degradation curtailed), even in the face of limited food intake or frank starvation, to provide sufficient quantities of these lipids to fulfill their crucial role in biologic membranes.In rodents the proportion of total body fatty acids synthesized by the liver ranges from 3% (fasted animals) to 50% (in animals force fed with glucose). 1 ' 2 Even greater percentages are synthesized in the human 3 and avian 4 liver. Dietary control of lipogenesis is more pronounced and more prompt in the liver than in any other tissue, further emphasizing the fact that the liver is of considerable importance as a lipogenic organ. 1 The rate of lipogenesis in mammalian liver is regulated by two types of mechanisms, distinguished by the time required for them to take effect. One involves long-term, adaptive changes in enzyme activity, due to fluctuations in the absolute amounts of the key lipogenic enzymes. 5 " 10 This type of regulation is subject to hormonal and nutritional factors and takes a few hours to come into effect. The other involves short-term mechanisms, which operate on a minute to minute basis. The latter, involving modulation of enzymatic activity by substrate supply, allosteric effectors, and interconversion of enzymes between active and inactive forms by a phosphorylation cycle, has not received as much attention as have the long-term adaptive changes of the lipogenic enzymes and is not as well understood as a means of regulating lipogenesis. In this review, we will focus attention on conditions and factors, e.g., hormones, that bring about rapid changes in the rate of hepatic lipogenesis;...

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Section: Hormonal Regulation Of Fatty Acid Oxidation and Complex Lipimentioning

confidence: 98%

Short-term Hormonal Control of Hepatic Lipogenesis

et al. 1980

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“…In recent reviews it is stated that there is no solid evidence for a rapid direct action of insulin when present as the sole hormone, on both glycogen synthesis (Hems 1978) and glycogenolysis (Hems and Whitton 1980) in the liver. On the other hand, it is well established that the glycogenolytic action of glucagon can be counteracted by insulin (Hems and Whitton 1980).…”

Section: Introductionmentioning

confidence: 99%

Control of Glycogen Metabolism by Insulin in Isolated Hepatocytes

Beynen¹,

Geelen²

1981

Horm Metab Res

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Isolated rat hepatocytes incubated in a simple bicarbonate buffer, previously shown to display enhanced rates of fatty acid biosynthesis upon a brief exposure to insulin, were used to study acute effects of this hormone on glycogen metabolism. In hepatocytes prepared from fed rats insulin does not increase glycogen deposition as measured chemically, but the incorporation of labelled glucose is markedly accelerated. The rate of disappearance of radioactivity from glycogen, prelabelled with D[U-14C]glucose, is lowered by insulin. In hepatocytes from starved rats insulin promotes net glycogen synthesis. All metabolic parameters studied are affected by glucagon in manner opposite to that of insulin.

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