Effect of dibutyryl cAMP on the enzymes of fatty acid synthesis and of glycogen metabolism

Rous, Simonne

doi:10.1016/0014-5793(70)80591-9

Cited by 13 publications

(7 citation statements)

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“…278 Identification of reductase kinase and the phosphatase established that a protein phosphorylation and dephosphorylation event accompanied the activation-inactivation of HMG-CoA reductase. The studies of Beg et al 281 confirmed this by showing a close correlation between inactivation of HMG-CoA reductase and 32 P| incorporation from [y 32 Pi]ATP into the enzyme. Similar results were obtained by Keith et al 284 and Gil et al 285 Reductase kinase is also an interconvertible enzyme.…”

Section: Hormonal Regulation Of Cholesterol Synthesissupporting

confidence: 50%

“…Reports that epididymal fat tissue, 111 chick liver cells, 112 and a purified rat liver fraction 113 can incorporate 32 Pj into carboxylase, without affecting enzyme activity, have been interpreted to mean that acetyl-CoA carboxylase is not controlled by phosphorylation and dephosphorylation mechanisms. These ostensibly contradictory observations may be explained by differences in extraction and assay procedures used by different investigators.…”

Section: Hormonal Regulation Of Fatty Acid Synthesismentioning

confidence: 97%

“…54 -55 For instance, exposure to cold temperatures, the natural tendency of the biochemist trying to preserve enzyme activity, leads to inactivation of rat liver acetyl-CoA carboxylase. 114>11S On the other hand, proteolysis, at least by tryspin, can result in activation of the enzyme 116 and, at the same time, might lead to 32 Pi loss. The activity of the enzyme is generally assayed after preincubation with citrate, which activates the enzyme.…”

Section: Hormonal Regulation Of Fatty Acid Synthesismentioning

confidence: 97%

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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 Cholesterol Synthesissupporting

confidence: 50%

Section: Hormonal Regulation Of Fatty Acid Synthesismentioning

confidence: 97%

Section: Hormonal Regulation Of Fatty Acid Synthesismentioning

confidence: 97%

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Short-term Hormonal Control of Hepatic Lipogenesis

et al. 1980

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“…Phosphatases counteract PKAmediated phosphorylation, terminating the cAMP signal (Khandelwal et al, 1976;Ingebritsen and Cohen, 1983). Evidence generated over the years shows that this pathway triggers a plethora of cellular effects, at times with opposing functional outcomes, including cell proliferation and differentiation (Stork and Schmitt, 2002); gene expression (Yamamoto et al, 1988); apoptosis (Weissinger et al, 1997;Suen et al, 2008); several metabolic processes, such as insulin secretion (Brisson et al, 1972), glycogen synthesis (Rous, 1970), and lipogenesis (Geelen and Vaartjes, 1977); and many others.…”

Section: Introductionmentioning

confidence: 99%

Subcellular Organization of the cAMP Signaling Pathway

2020

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“…Thus there is controversy about the action of glucagon on hepatic fatty acid synthesis. A series of reports have suggested that glucagon or cyclic AMP can inhibit fatty acid synthesis in the rodent liver, on the basis of experiments with intact rats (Rous, 1970;Klain & Weiser, 1973), liver slices (Haugaard & Stadie, 1953;Bloxham & Akhtar, 1972;Akhtar & Bloxham, 1970;Allred & Roehrig, 1973;Bricker & Levey, 1972a,b;Bricker & Marraccini, 1975;Meikle et al, 1974;Raskin et al, 1974) or cell suspensions (Capuzzi et al, 1971(Capuzzi et al, , 1974Harris, 1975;Edwards, 1975;Muller et al, 1976). But studies with the perfused rat liver have been less conclusive.…”

mentioning

confidence: 99%

Effects of glucagon and insulin on fatty acid synthesis and glycogen degradation in the perfused liver of normal and genetically obese (ob/ob) mice

Y¹,

Gove²,

Hems³

1978

Biochemical Journal

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1. Rapid effects of hormones on glycogen metabolism and fatty acid synthesis in the perfused liver of the mouse were studied. 2. In perfusions lasting 2h, of livers from normal mice, glucagon in successive doses, each producing concentrations of 10(-10) or 10(-9)M, inhibited fatty acid and cholesterol synthesis. In perfusions lasting 40–50 min, in which medium was not recycled, inhibition of fatty acid synthesis was only observed with glucagon at concentrations greater than 10(-9)M. This concentration was about two orders of magnitude higher than that required for the stimulation of glycogen breakdown. Glucagon did not inhibit the activity of acetyl-CoA carboxylase, assayed 10 or 20 min after addition of glucagon (10(-9) or 10(-10)M). It is proposed that the action of glucagon on hepatic fatty acid biosynthesis could be secondary in time to depletion of glycogen. Insulin prevented the effect of glucagon (10(-10)M) on glycogenolysis, but not that of vasopressin. 3. Livers of genetically obese (ob/ob) mice did not show significant inhibition of lipid biosynthesis in response to glucagon, although there was normal acceleration of glycogen breakdown. This resistance to glucagon action was not reversed by food deprivation. Livers of obese mice exhibited resistance to the counteraction by insulin of glucagon-stimulated glycogenolysis, which was reversible by partial food deprivation.

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Effect of dibutyryl cAMP on the enzymes of fatty acid synthesis and of glycogen metabolism

Cited by 13 publications

References 10 publications

Short-term Hormonal Control of Hepatic Lipogenesis

Short-term Hormonal Control of Hepatic Lipogenesis

Subcellular Organization of the cAMP Signaling Pathway

Effects of glucagon and insulin on fatty acid synthesis and glycogen degradation in the perfused liver of normal and genetically obese (ob/ob) mice

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