The role of brown adipose tissue in diet-induced thermogenesis

Stock, Michael J.

doi:10.1079/pns19890029

Cited by 22 publications

(17 citation statements)

References 47 publications

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“…Feed efficiency, a measure of metabolic function (19,20), was negative in the melatonin-treated animals and positive in controls; this effect was immediately reversed when the treatments were crossed over. These results suggest that melatonin may alter either metabolism or the ability to store excess energy as body fat, and that this effect is readily reversible.…”

Section: Discussionmentioning

confidence: 94%

Daily Melatonin Administration to Middle-Aged Male Rats Suppresses Body Weight, Intraabdominal Adiposity, and Plasma Leptin and Insulin Independent of Food Intake and Total Body Fat1

et al. 2000

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Pineal melatonin secretion declines with aging, whereas visceral fat, plasma insulin, and plasma leptin tend to increase. We have previously demonstrated that daily melatonin administration at middle age suppressed male rat intraabdominal visceral fat, plasma leptin, and plasma insulin to youthful levels; the current study was designed to begin investigating mechanisms that mediate these responses. Melatonin (0.4 g/ml) or vehicle was administered in the drinking water of 10-month-old male Sprague Dawley rats (18/treatment) for 12 weeks. Half (9/treatment) were then killed, and the other half were submitted to cross-over treatment for an additional 12 weeks. Twelve weeks of melatonin treatment decreased (P Ͻ 0.05) body weight (BW; by 7% relative to controls), relative intraabdominal adiposity (by 16%), plasma leptin (by 33%), and plasma insulin (by 25%) while increasing (P Ͻ 0.05) locomotor activity (by 19%), core body temperature (by 0.5 C), and morning plasma corticosterone (by 154%), restoring each of these parameters toward more youthful levels. Food intake and total body fat were not changed by melatonin treatment. Melatonin-treated rats that were then crossed over to control treatment for a further 12 weeks gained BW, whereas control rats that were crossed to melatonin treatment lost BW, but food intake did not change in either group. Feed efficiency (grams of BW change per g cumulative food intake), a measure of metabolic function, was negative in melatonin-treated rats and positive in control rats before cross-over (P Ͻ 0.001); this relationship was reversed after cross-over (P Ͻ 0.001). Thus, melatonin treatment in middle age decreased BW, intraabdominal adiposity, plasma insulin, and plasma leptin, without altering food intake or total adiposity. These results suggest that the decrease in endogenous melatonin with aging may alter metabolism and physical activity, resulting in increased BW, visceral adiposity, and associated detrimental metabolic consequences. (Endocrinology 141: [487][488][489][490][491][492][493][494][495][496][497] 2000) T HE PINEAL GLAND secretes melatonin into the circulation almost entirely at night in vertebrates (1, 2). This nocturnal secretion mediates entrainment of endogenous circadian rhythms and influences other physiological functions. Pineal melatonin biosynthesis and secretion decline with aging; levels are significantly decreased by middle age (2, 3) and tend to decline throughout old age.Adiposity, especially visceral adiposity, increases with advancing age in humans (4), nonhuman primates (5, 6), and rats (7), as do plasma insulin and leptin levels. These changes in adiposity, insulin, and leptin levels are often associated with detrimental metabolic consequences, such as glucose intolerance, insulin resistance, diabetes, dyslipidemia, and hypertension (4,5,8). We have previously demonstrated that daily nocturnal melatonin administration to middle-aged male rats suppressed intraabdominal (commonly referred to as deep abdominal or visceral) fat, plasma leptin...

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Section: Discussionmentioning

confidence: 94%

Daily Melatonin Administration to Middle-Aged Male Rats Suppresses Body Weight, Intraabdominal Adiposity, and Plasma Leptin and Insulin Independent of Food Intake and Total Body Fat1

et al. 2000

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“…BAT was shown to be involved in diet-induced thermogenesis [29,30], and it is possible that diet-induced thermogenesis was also decreased due to the changes in UCP-1 expression in BAT and in BAT mass. Another possible explanation for the decreased energy expenditure in the MCH-treated animals is a decrease in their physical activity.…”

Section: Discussionmentioning

confidence: 97%

Chronic MCH infusion causes a decrease in energy expenditure and body temperature, and an increase in serum IGF-1 levels in mice

Glick

Segal-Lieberman

Cohen

et al. 2009

Endocr

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Melanin concentrating hormone (MCH) is an orexigenic peptide secreted from the lateral hypothalamus. Various observations suggest a role for MCH in energy expenditure in transgenic mice; however, the influence of MCH on energy expenditure and body temperature in WT mice was inadequately studied. Therefore, our first goal was to characterize the influence of chronic intracerebroventrical MCH infusion on energy homeostasis in mice. Our second goal was to explore the effect of MCH on the GH-insulin like growth factor 1 (IGF-1) axis in vivo. We have recently published that MCH directly increased GH-secretion from pituitary cells in vitro, suggesting that MCH may exert part of its effects on energy balance via direct pituitary hormone regulation. Mice were centrally infused with MCH for 14 days, resulting in a significant increase in food intake, body weight, fat mass and plasma IGF-1 levels, while decreasing body temperature and energy expenditure. Our data emphasize the role of MCH as a key regulator of energy homeostasis by means of appetite regulation, regulation of energy expenditure, and an integrator of energy balance with the neuroendocrine system regulating pituitary hormone secretion. They also support the notion that MCH may have a physiologic role in GH regulation that may, in turn, contribute to its effect on body weight.

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“…Stock and Rothwell (962) showed that brown adipose tissue played a role in the response to these diets by dissipating additional calories rather than storing them. In the animal that has overeaten a highly palatable diet, the thermogenic response to NE is accentuated, and is blocked by propran- olol, indicating that ␤-adrenergic receptors are involved (962). Studies of the mitochondria from brown adipose tissue revealed that it has a functional proton leak that could be activated by NE.…”

Section: ␤ 3 -Adrenergic Agonistsmentioning

confidence: 97%

“…One site of action for this response is brown adipose tissue (962). This tissue is abundant in newborn animals and is believed to be important in maintaining thermoregulation in the newborn (959).…”

Section: ␤ 3 -Adrenergic Agonistsmentioning

confidence: 99%