Involvement of a humoral factor in regulation of body weight in parabiotic rats

Parameswaran, S. V.; Steffens, A.B.; Hervey, G. R.; Ruiter, L. de

doi:10.1152/ajpregu.1977.232.5.r150

Cited by 33 publications

(41 citation statements)

References 14 publications

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“…Parabiosis experiments with obese mice (1, 2) or rats (3,4) demonstrated the involvement of circulating factors as feedback signals in the regulation of energy balance. Zhang et al (5) recently used positional cloning to identify one such potential signal that is mutated in genetically obese ob/ob mice.…”

Section: Introductionmentioning

confidence: 99%

Early and late stimulation of ob mRNA expression in meal-fed and overfed rats.

Harris¹,

Ramsay²,

Smith³

et al. 1996

J. Clin. Invest.

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Abstractob protein is hypothesized to be a circulating feedback signal in the regulation of energy balance. Obese, overfed rats have high levels of ob mRNA expression and suppressed voluntary food intake, indicating the presence of a potent satiety factor. The objectives of this experiment were to determine whether feeding rats their normal daily intake in three meals, compared with ad libitum feeding, increased ob mRNA expression and to determine the degree of obesity required to stimulate expression of ob mRNA. Rats were fed ad libitum, were tube-fed their normal intake in three meals a day, or were tube-fed twice normal intake. ob mRNA was measured by Northern blot analysis after 0, 2, 7, 14, 21, and 32 d of tube-feeding. After only 2 d ob mRNA was threefold higher in tube-fed animals than in ad libitum controls. By day 21 there was a further increase in ob mRNA expression in overfed rats which were at 130% control weight. These results suggest that a metabolic consequence of meal-feeding increases ob mRNA expression in the absence of increased food intake or weight gain. There is a further increase in ob mRNA expression once significant obesity is

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Section: Introductionmentioning

confidence: 99%

Early and late stimulation of ob mRNA expression in meal-fed and overfed rats.

Harris¹,

Ramsay²,

Smith³

et al. 1996

J. Clin. Invest.

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“…The existence of a factor secreted in proportion to energy stores in WAT, which acts in the brain to control feeding, weight and WAT mass, was first proposed by Kennedy (16) and is supported by the discovery of monogenic mutations resulting in obesity, as well as classic cross-circulation (parabiosis) experiments in rodents (17)(18)(19)(20). The list of adipocytokines known to affect metabolism keeps growing (Table 1).…”

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confidence: 99%

Brain Adipocytokine Action and Metabolic Regulation

et al. 2006

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Adipose tissue secretes factors that control various physiological systems. The fall in leptin during fasting mediates hyperphagia and suppresses thermogenesis, thyroid and reproductive hormones, and immune system. On the other hand, rising leptin levels in the fed state stimulate fatty acid oxidation, decrease appetite, and limit weight gain. These divergent effects of leptin occur through neuronal circuits in the hypothalamus and other brain areas. Leptin also regulates the activities of enzymes involved in lipid metabolism, e.g., AMP-activated protein kinase and stearoyl-CoA desaturase-1, and also interacts with insulin signaling in the brain. Adiponectin enhances fatty acid oxidation and insulin sensitivity, in part by stimulating AMP-activated protein kinase phosphorylation and activity in liver and muscle. Moreover, adiponectin decreases body fat by increasing energy expenditure and lipid catabolism. These effects involve peripheral and possibly central mechanisms. Adipose tissue mediates interconversion of steroid hormones and secretes proinflammatory cytokines, vasoactive peptides, and coagulation and complement proteins. Understanding the actions of these "adipocytokines" will provide insight into the pathogenesis and treatment of obesity and related diseases. Diabetes 55 (Suppl. 2): S145-S154, 2006 ADIPOSE TISSUE

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“…Stimulation of the LH induces stimulus-bound feeding and weight gain. 18 In contrast, lesions in the LH produce a characteristic acute hypophagia 19 and an increase in the activity of the SNS, 20,21 which is followed by permanent reduction in body weight. Hypophagia after an LH lesion (or treatment with fen¯uramine) does not occur if the weight of the test subjects is acutely reduced by food restriction to a level below what would be achieved after the lesion or drug treatment.…”

Section: The Sympathetic Nervous System and Food Intake: Experimentalmentioning

confidence: 99%

True

2000

Int J Obes

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The neuropeptides, monoamines and many drugs involved with modulating food intake and fat stores have reciprocal effects on sympathetic activity and thermogenesis. Both serotonin, acting through 5HT 1Ba2C receptors, and norepinephrine acting through b b 2 andaor b b 3 receptors reduce food intake and augment sympathetic activity. Neuropeptide Y, b b-endorphin, orexin, galanin and melanin concentrating hormone all increase food intake and, where tested, reduce sympathetic activity. In contrast, a larger number of peptides including cholecystokinin, corticotrophin-releasing hormoneaurocortin, enterostatin, leptin, CART and a-MSH reduce food intake and increase sympathetic activity. Nicotine, prostaglandin, dexfen¯uramine and sibutramine also have this reciprocal effect on feeding and sympathetic nervous system (SNS) activity. Chronic administration of neuropeptide Y (NPY) can produce chronically increased food intake and obesity. This syndrome is similar to the ventromedial hypothalamus (VMH) syndrome and suggests that NPY must be acting as an inhibitory signal to stimulate a feeding system and inhibit sympathetic activity. The melanocortin receptor system may be particularly important in modulating food intake, because a transgenic mouse which does not express melanocortin-4 receptors is massively overweight. Adrenal glucocorticoids are important in obesity since adrenalectomy will reverse or prevent the development of all forms of obesity. The clinical importance of the sympathetic nervous system and food intake is emphasized by the inverse relation of sympathetic activity and body fat. The inhibition of food intake, lower body fat stores and higher energy expenditure in smokers also support this hypothesis. The reciprocal relationship between food intake and sympathetic activity is robust, suggesting that b b receptors in the periphery and brain may be involved in the control of feeding and a reduction in food intake in humans accounts for most of the weight loss with ephedrine and caffeine. We conclude that the inhibition of feeding by activating the SNS is an important satiety system which helps regulate body fat stores.

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Involvement of a humoral factor in regulation of body weight in parabiotic rats

Cited by 33 publications

References 14 publications

Early and late stimulation of ob mRNA expression in meal-fed and overfed rats.

Early and late stimulation of ob mRNA expression in meal-fed and overfed rats.

Brain Adipocytokine Action and Metabolic Regulation

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