Decreased guanine nuleotide binding and reduced equivalent production by brown adipose tissue in hypothalamic obesity

Seydoux, J; Ricquier, Daniel; Rohner‐Jeanrenaud, Françoise; Assimacopoulos-Jeannet, F.; Giacobino, Jean‐Paul; Jeanrenaud, B.; Girardier, L

doi:10.1016/0014-5793(82)80726-6

Cited by 34 publications

(5 citation statements)

References 17 publications

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“…Secondly, the impaired thermogenesis is unlikely to be secondary to the hyperphagia of obese rats. The decrease in GDP binding in rats made obese by hypothalamic lesions was prevented by restriction of food intake (Seydoux et al, 1982). This effect, it was suggested, was mediated through regulatory changes in the sympathetic nervous system.…”

Section: Discussionmentioning

confidence: 95%

The effects of corticosterone, cold exposure and overfeeding with sucrose on brown adipose tissue of obese Zucker rats (fa/fa)

Holt¹,

York²,

Fitzsimons³

1983

Biochemical Journal

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GDP binding to brown-adipose-tissue mitochondria was decreased in obese Zucker rats. Adrenalectomy restored both GDP binding and serum tri-iodothyronine of obese rats to values observed in lean rats. The effects of adrenalectomy on GDP binding and serum tri-iodothyronine were reversed by corticosterone. Decreasing food intake had no effect on brown-adipose-tissue GDP binding in obese rats. Young (5-week-old) obese rats showed a normal increase in brown-adipose-tissue mitochondrial GDP binding after housing at 4 degrees C for 7 days, but this response was attenuated in 10-week-old obese rats. Overfeeding with sucrose increased brown-adipose-tissue thermogenesis in lean, but not in obese, rats. After adrenalectomy, overfeeding with sucrose enhanced brown-adipose-tissue mitochondrial GDP binding in obese rats.

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Section: Discussionmentioning

confidence: 95%

The effects of corticosterone, cold exposure and overfeeding with sucrose on brown adipose tissue of obese Zucker rats (fa/fa)

Holt¹,

York²,

Fitzsimons³

1983

Biochemical Journal

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“…Inhibition of thermogenesis following surgical or chemical destruction of the VMH has been inferred from increases in the efficiency of weight gain (Han et al 1965; Han, lm), reduction in the acute thermogenic responses to food (Carlisle et al 1988), in noradrenaline turnover and thermogenic activity of brown fat (Seydoux et al 1981; Hogan et al 1982; Yoshida et al 1983;Niijima et al 1984) all of which are reduced and probably contribute to the development of obesity. Once again it is difficult to distinguish the influence on thermogenesis of the VMH from that of the VNAB.…”

Section: Increased: Lipgenesis-lipolysis In Batmentioning

confidence: 99%

Central control of brown adipose tissue

Rothwell

1989

Proc. Nutr. Soc.

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Thermogenesis is a term which can be used to describe any form of heat production, but is normally applied to adaptive or regulatory components of metabolic rate, namely non-shivering thermogenesis (NST) and diet-induced thermogenesis (DIT). NST and DIT are activated in response to physiological stimuli and are largely dependent on sympathetic activation of heat production in brown adipose tissue (BAT). The quantitative importance and thermogenic mechanisms of BAT will be reviewed by others participating in this symposium. The objective of the present review is to discuss our current knowledge of the central mechanisms involved in the control of BAT thermogenesis, and how they are affected by physiological or pathological conditions.Of all aspects of BAT thermogenesis it is the central control which is probably the least understood, partly as a result of its complexity, but also because it has received relatively little direct attention. Considerable information and insight into this area can, however, be gained from studies concerned with feeding behaviour and temperature regulation, both of which are closely related and show many common features with sympatheticallymediated thermogenesis. Over the past few years, our understanding of central thermogenic mechanisms has improved considerably, due mainly to studies specifically designed to investigate this problem. Areas of the brain controlling BATThe hypothalamus is the major area concerned with the control of autonomic functions, particularly feeding behaviour and thermoregulation, and has been the primary focus for studies on BAT thermogenesis. A close association between the ventromedial hypothalamus (VMH) and the regulation of body-weight or energy balance was first demonstrated almost 40 years ago, when destruction of the ventromedial nucleus was shown to result in hyperphagia and obesity. For a long time thereafter the VMH was referred to as a 'satiety' centre, acting reciprocally with the lateral hypothalamus (LH; known as the hunger centre) to control food intake (Stellar, 1954). However, obesity will develop in response to VMH lesions in the absence of hyperphagia, indicating that energy expenditure was simultaneously reduced (Han et al.

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“…The GDP binding sites are increased in high thermogenic states like cold acclimation [ 181 or spontaneous overfeeding [ 191 and decreased in low thermogenic states like warmadaptation [20] or genetic or experimentally induced obesity [21,22]. The 32000 Mr protein is increased in cold acclimation [9,10,18] and decreased in warm adaptation [9,23] and in experimentally induced obesity associated with overfeeding [22]. In diabetes, a state where BAT thermogenesis is reduced [5], both GDP-binding and 32000 M, protein are significantly decreased as compared to the control which is another indication that these two parameters are indices of the thermogenic capacity of BAT.…”

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confidence: 99%

Modulation of β‐oxidation and proton conductance pathway of brown adipose tissue in hypo‐ and hyperinsulinemic states

Seydoux¹,

Trimble²,

Bouillaud

et al. 1984

FEBS Letters

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The metabolic capacity of interscapular brown adipose tissue of hypoinsulinemic (diabetic) rats is decreased and a reduced &oxidative capacity contributes to this metabolic alteration. It was thus of interest to compare, in diabetic and in chronically (8 days) insulin-infused rats, the &oxidative capacity and indices of the thermogenic state (GDP-binding and 32000 A4, protein) in this tissue. Mitochondrial GDP-binding and 32000 IV, protein were both decreased in diabetic rats compared to appropriate controls and markedly increased as was also the fl-oxidative capacity in hyperinsulinemic rats.

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Decreased guanine nuleotide binding and reduced equivalent production by brown adipose tissue in hypothalamic obesity

Cited by 34 publications

References 17 publications

The effects of corticosterone, cold exposure and overfeeding with sucrose on brown adipose tissue of obese Zucker rats (fa/fa)

The effects of corticosterone, cold exposure and overfeeding with sucrose on brown adipose tissue of obese Zucker rats (fa/fa)

Central control of brown adipose tissue

Modulation of β‐oxidation and proton conductance pathway of brown adipose tissue in hypo‐ and hyperinsulinemic states

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