Role of Cyclic-3′,5′-Amp in the Response of Adipose Tissue to Insulin

Jungas, Robert L.

doi:10.1073/pnas.56.2.757

Cited by 149 publications

(37 citation statements)

References 20 publications

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“…As does nicotinic acid, insulin is supposed to have a decreasing effect on cyclic AMP levels [14] by acting both on adenylate cyclase and on phosphodiesterase [29]. Although the mechanism of action of the two drugs is not the same we observed a similar effect of both drugs on white and brown adipocytes.…”

Section: Discussionsupporting

confidence: 66%

Effects of Lipolytic and Antilipolytic Drugs on Metabolism of Adenosine 3′: 5′‐Monophosphate in Brown Adipose Tissue of Cold Acclimated Rats

Bertin

Portet

1976

European Journal of Biochemistry

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The intracellular level of adenosine 3' : 5'-monophosphate (cyclic AMP) and its stimulation in vitro by norepinephrine were studied in brown and white adipocytes from rats adapted to constant or fluctuating cold. Cold acclimatization had no effect on the basal cyclic AMP intracellular content in both tissues, but the level in brown adipocytes was four-fold higher than in the white ones. Addition of norepinephrine in the incubation medium doubled the cyclic AMP content of white adipocytes from control or fluctuating-cold-adapted rats, and enhanced four-fold in constant-cold-adapted rats. In brown adipocytes norepinephrine increased cyclic AMP levels in the first two groups, but had no effects in constant-cold-adapted rats. In the two tissues of control and fluctuating-cold-adapted rats the norepinephrine action was increased by phentolamine and decreased by propranolol. The lack of response to norepinephrine of brown adipocytes from constant cold-adapted rats was not due to the predominance of the CI component of hormone receptors. Antilipolytic drugs (nicotinic acid, insulin and prostaglandin E2) inhibited the action of norepinephrine on white adipocytes ; only prostaglandin E 2 had an effect on brown ones.Brown adipose tissue which is hypertrophied in cold-adapted animals could be involved in the nonshivering thermogenesis regulation. Heat production is generally regarded as a very important characteristic of interscapular brown adipose tissue in which norepinephrine-mediated triglyceride hydrolysis seems to have an essential role [1,2]. As a matter of fact coldadapted rats are hypersensitive to the calorigenic action of that hormone [3,4]. In incubated brown adipocytes from cold-adapted rats there is also an increased response of 0 2 consumption with norepinephrine addition [ 5 ] ; however in the same time, lipolysis is not increased by the hormone [6,7]. This fact is surprising since it is known that in this tissue, lipid metabolism is very important as shown by experiments in vivo [8]. Cyclic AMP is regarded as the intracellular mediator of lipolytic hormones in white adipocytes [9] but there is only little information on cyclic AMP mediation in brown ones [lo]. We have previously found [ll] that in brown adipocytes from cold-adapted hamsters, norepinephrine does not stimulate cyclic AMP production. However in that 'pseudo hibernator' the hormonal regulation of lipolysis could be quite different from the regulation in strict homeotherm. Moreover we have found in rats __ --Ahbrewation. Cyclic AMP, adenosine 3': 5'-monophosphate.that hormonal production is differently modified whether the animals are maintained to constant cold or submitted to nycthemeral variations of temperature [12]. The aim of this study is to study comparatively in brown and white adipocytes from constant or fluctuating-cold-acclimated rats the effect of lipolytic hormones and antilipolytic agents on cyclic AMP intracellular production. MATERIALS AND METHODS Exper imen i d ConditionsAll the experiments were performed on male Long Evans r...

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Section: Discussionsupporting

confidence: 66%

Effects of Lipolytic and Antilipolytic Drugs on Metabolism of Adenosine 3′: 5′‐Monophosphate in Brown Adipose Tissue of Cold Acclimated Rats

Bertin

Portet

1976

European Journal of Biochemistry

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“…3 to fluoride stimulation could be observed (table 2). Furthermore, when a different preparation (NSILA-S I) was inactivated by reduction and aminoethylatron, it had also lost its effect on the adenyl cyclase system.…”

Section: Experiments IImentioning

confidence: 93%

Inhibition of glucagon‐stimulated adenyl cyclase by insulin

Hepp

1971

FEBS Letters

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“…However, a lack of effect of insulin in vitro or in vivo on the activity of phosphodiesterase has been observed for the rat liver [25,66] and adipose tissue enzyme [48,66,67]. Although after incubation of the tissue with hormone a decrease in cyclase activity has been observed by prior incubation [68], a direct effect of insulin on this enzyme in adipose tissue homogenate is lacking [68,69]. An effect on membrane configuration has also been suggested by Rodbell [70] as a possible mechanism of insulin action.…”

Section: Effects Of Insulin and Buado-3' :5'-p On Endogenous Liver Mmentioning

confidence: 99%

Interactions of Glucagon and Insulin on the Metabolism of Perfused Livers from Fasted Rats

Menahan

Wieland²

1969

European Journal of Biochemistry

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Glucagon (28 nM) stimulated gluconeogenesis, urea production and ketogenesis in perfused livers from fasted rats. Since the livers were perfused without added substrate, liver protein is the source of carbon of the glucose synthesis. Addition of N6, O2′‐dibutyryl cyclic adenosine 3′:5′‐monophosphate in concentrations of 100 and 10 μM to the perfusion medium resulted in a response similar to that of glucagon. It is suggested that cyclic adenosine 3′:5′‐monophosphate is the mediator of glucagon action in liver. Preperfusion of the isolated livers with insulin diminished the glucagon effects. The glucagon‐stimulation of glucose and urea production was completely suppressed, while the increased ketogenesis was inhibited by 60% in the presence of insulin. Since all three glucagon responses were inhibited, this supports the concept that insulin lowers, in some way, the elevation of cyclic adenosine 3′:5′‐phosphate which occurs following glucagon administration. That insulin does not exert its effect subsequent to cyclic adenosine 3′:5′‐phosphate is suggested by the observation that insulin, under the same conditions which inhibited the response of liver to glucagon, had little or no effect on the increases in gluconeogenesis, ureogenesis, and ketogenesis following, dibutyryl cyclic adenosine‐3′:5′‐phosphate. Since an effect of insulin on cyclic adenosine 3′:5′‐phosphate phosphodiesterase seems unlikely, it is suggested that the inhibition of glucagon responses by insulin is the result of an interaction at the adenyl cyclase or one of the step(s) between binding of the hormone and the enzyme.

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Role of Cyclic-3′,5′-Amp in the Response of Adipose Tissue to Insulin

Cited by 149 publications

References 20 publications

Effects of Lipolytic and Antilipolytic Drugs on Metabolism of Adenosine 3′: 5′‐Monophosphate in Brown Adipose Tissue of Cold Acclimated Rats

Effects of Lipolytic and Antilipolytic Drugs on Metabolism of Adenosine 3′: 5′‐Monophosphate in Brown Adipose Tissue of Cold Acclimated Rats

Inhibition of glucagon‐stimulated adenyl cyclase by insulin

Interactions of Glucagon and Insulin on the Metabolism of Perfused Livers from Fasted Rats

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