Effects of diet and photoperiod on NE turnover and GDP binding in Siberian hamster brown adipose tissue

1986 ◽  
Vol 250 (3) ◽  
pp. R383-R388 ◽  
Author(s):  
J. F. McElroy ◽  
P. W. Mason ◽  
J. M. Hamilton ◽  
G. N. Wade
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Turnover Rate ◽  
Siberian Hamsters ◽  
Bat Mitochondria ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis ◽  
Long Photoperiod

This experiment examined the effects of diet and photoperiod on food intake, body weight, and brown adipose tissue (BAT) activity in female Siberian hamsters (Phodopus sungorus sungorus). BAT function was assessed by measuring both the sympathetic nervous system activity of BAT [estimated by the rate of norepinephrine (NE) turnover] and BAT thermogenic activity (estimated by GDP binding to BAT mitochondria). Nineteen weeks of high-fat feeding in long photoperiod [16:8 light-dark cycle (LD)] caused a 20% increase in food intake but did not affect body weight. Both NE turnover rate and GDP binding in interscapular BAT (IBAT) were increased four- to eightfold relative to that from chow-fed controls. Thus it appears that in Siberian hamsters BAT can serve the same energy-dissipating function during diet-induced overeating previously established in rats and mice. Nineteen-week exposure to a short photoperiod (LD 8:16) produced a reduction in body weight but did not affect food intake. Both NE turnover rate and GDP binding in IBAT were increased two- to fourfold relative to that from long-photoperiod controls. Thus it appears that in Siberian hamsters the photoperiod-induced improvements in thermogenic capacity are mediated via the same mechanisms as are cold- or diet-induced thermogenesis.

Relationship of brown adipose tissue with growth and obesity differences in genetically selected mouse lines

1984 ◽  
Vol 26 (3) ◽  
pp. 339-347 ◽  
Author(s):  
A. M. Saxton ◽  
E. J. Eisen ◽  
J. M. Leatherwood
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Single Gene ◽  
Tissue Growth ◽  
Growth Patterns ◽  
High Fat ◽  
Polygenic Control ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis

A recent hypothesis considers brown adipose tissue (BAT) to be an important source of diet-induced thermogenesis (DIT). In turn, DIT and thermogenesis in general are believed to be key factors in the control of obesity of laboratory rodents. This hypothesis was developed from the study of single gene mutant obese rodents. The present research tested this hypothesis in mice with polygenic control of growth and obesity, which is more characteristic of the type of genetic variation expected in human and other mammalian populations. Control and high fat diets were used to test responses of five genetically selected lines of mice showing different patterns of growth and obesity. All lines deposited more fat on the high fat diet, but the most obese line showed the largest increase in BAT and the lipid-free dry (LFD) component of BAT. Use of LFD per unit body weight gave results which supported the hypothesis being tested, but it was argued that this measure is misleading. When brown and white adipose tissue growth relative to body weight were examined, 2 of the 10 line – diet groups showed alterations in BAT growth patterns. However, it was concluded that BAT, if involved at all, was not a major factor in growth and obesity differences.Key words: obesity, polygenes, adipose tissue, quantitative inheritance, mouse.

Brown adipose tissue thermogenesis in testosterone-treated rats

1992 ◽  
Vol 126 (5) ◽  
pp. 434-437 ◽  
Author(s):  
María Abelenda ◽  
Maria Paz Nava ◽  
Alberto Fernández ◽  
María Luisa Puerta
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Male Rats ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Sexual Hormones ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

The participation of sexual hormones in body weight regulation is partly accomplished by altering food intake. Nonetheless, female sexual hormones also alter brown adipose tissue thermogenesis in females. This study was aimed to find out if male hormones could alter brown adipose tissue thermogenesis in male rats. Testosterone was administered by means of Silastic capsules in adult male rats acclimated either at 28°C (thermoneutrality) or at 6°C (cold), treatment lasting 15 days. Food intake and body weight gain were reduced by hormonal treatment. However, brown adipose tissue mass, protein content, mitochondrial mass and GDP-binding were unchanged at both environmental temperatures. Accordingly, testosterone participation in body weight regulation is thought to be carried out without altering brown adipose tissue thermogenesis. A reduction in the weight of the sex accessory glands was also observed after cold acclimation.

scholarly journals Intact innervation is essential for diet-induced recruitment of brown adipose tissue

2019 ◽  
Vol 316 (3) ◽  
pp. E487-E503 ◽  
Author(s):  
Alexander W. Fischer ◽  
Christian Schlein ◽  
Barbara Cannon ◽  
Joerg Heeren ◽  
Jan Nedergaard
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Chow Diet ◽  
Metabolic Efficiency ◽  
Protein Levels ◽  
Brown Adipose ◽  
Ucp1 Expression ◽  
Diet Induced Thermogenesis

The possibility that recruitment and activation of brown adipose tissue (BAT) thermogenesis could be beneficial for curtailing obesity development in humans prompts a need for a better understanding of the control of these processes [that are often referred to collectively as diet-induced thermogenesis (DIT)]. Dietary conditions are associated with large changes in blood-borne factors that could be responsible for BAT recruitment, but BAT is also innervated by the sympathetic nervous system. To examine the significance of the innervation for DIT recruitment, we surgically denervated the largest BAT depot, i.e., the interscapular BAT depot in mice and exposed the mice at thermoneutrality to a high-fat diet versus a chow diet. Denervation led to an alteration in feeding pattern but did not lead to enhanced obesity, but obesity was achieved with a lower food intake, as denervation increased metabolic efficiency. Conclusively, denervation totally abolished the diet-induced increase in total UCP1 protein levels observed in the intact mice, whereas basal UCP1 expression was not dependent on innervation. The denervation of interscapular BAT did not discernably hyper-recruit other BAT depots, and no UCP1 protein could be detected in the principally browning-competent inguinal white adipose tissue depot under any of the examined conditions. We conclude that intact innervation is essential for diet-induced thermogenesis and that circulating factors cannot by themselves initiate recruitment of brown adipose tissue under obesogenic conditions. Therefore, the processes that link food intake and energy storage to activation of the nervous system are those of significance for the further understanding of diet-induced thermogenesis.

Brown adipose tissue in genetically obese (fa/fa) rats: response to cold and diet

1983 ◽  
Vol 244 (2) ◽  
pp. E145-E150 ◽  
Author(s):  
J. Triandafillou ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cafeteria Diet ◽  
Chow Diet ◽  
Purine Nucleotides ◽  
Noradrenaline Content ◽  
Bat Mitochondria ◽  
Brown Adipose ◽  
Consequent Reduction ◽  
Diet Induced Thermogenesis

Young genetically obese (fatty, fa/fa) rats (7-8 wk old) maintained on a chow diet at 28 degrees C have a relatively normal amount of brown adipose tissue (BAT) (normal protein content, normal noradrenaline content, normal or slightly reduced cytochrome oxidase content, 30% reduction in DNA content) with cells grossly hypertrophied by accumulation of lipid. The binding of purine nucleotides by BAT mitochondria is lower in fa/fa rats than in lean rats, suggesting a lesser thermogenic activation of this tissue. Acute exposure to cold (24 h at 4 degrees C) activates BAT thermogenesis (visible hyperemia, marked increase in mitochondrial binding of purine nucleotides, depletion of noradrenaline content) in fa/fa rats as in lean rats. In contrast, feeding a cafeteria diet to young fa/fa rats fails to activate BAT (no increase in mitochondrial binding of purine nucleotides) as it does in lean rats, and these rats accumulate more extra fat (increase in weight of gonadal white adipose tissue) than do cafeteria diet-fed lean rats. It is concluded that the young fa/fa rat has normal cold-induced nonshivering thermogenesis in BAT but defective diet-induced thermogenesis in BAT and that the consequent reduction in energy expenditure, coupled with hyperphagia, contributes to the development of its obesity. The most probable location for the defect is suggested to be associated with the hypothalamus.

Increased sensitivity of the genetically obese mouse to corticosterone

1987 ◽  
Vol 252 (2) ◽  
pp. E202-E208 ◽  
Author(s):  
K. Tokuyama ◽  
J. Himms-Hagen
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Obese Mouse ◽  
Serum Corticosterone ◽  
Brown Adipose

Adrenalectomy normalizes many abnormalities of the obese (ob/ob) mouse. The high corticosterone concentration in blood may account in part for development of obesity and other abnormalities in the ob/ob mouse. Our objective was to determine dose-response relationships for the effect of corticosterone on the obesity. Lean and ob/ob mice were adrenalectomized or sham-operated at 4.5 wk of age. Adrenalectomized mice received 100 mg implants of cholesterol containing corticosterone (0, 2, 5, 20, or 50 mg) at 8.5 wk of age and were killed at 10.5 wk of age. In ob/ob mice, but not in lean mice, low physiological levels of serum corticosterone (up to 10 micrograms/dl) markedly increased body weight gain, food intake, and serum insulin. They also increased white and brown adipose tissue weights and decreased brown adipose tissue mitochondrial GDP binding. Higher levels of corticosterone (12-22 micrograms/dl) increased body weight gain, white and brown adipose tissue weights, and serum insulin and suppressed brown adipose tissue mitochondrial GDP binding in lean mice also, although in most cases to a lesser extent than in ob/ob mice, but were still without effect on food intake. Only very high levels of corticosterone (approximately 30 micrograms/dl) increased food intake in lean mice. Hyperglycemia was induced in ob/ob, but not lean, mice only at concentrations of corticosterone greater than 17 micrograms/dl. Thermoregulation was unaffected by serum corticosterone at levels from 0 to 30 micrograms/dl in both ob/ob and lean mice. Thus the ob/ob mouse is excessively sensitive and responsive to an effect of physiological levels of corticosterone that results in hyperphagia, hyperinsulinemia, and increased weight gain.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Thermogenesis challenges the adipostat hypothesis for body-weight control

2009 ◽  
Vol 68 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Barbara Cannon ◽  
Jan Nedergaard
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Weight Control ◽  
Dietary Intervention ◽  
Human Subjects ◽  
Brown Adipose ◽  
Body Weight Control

According to the adipostat hypothesis for body-weight control, alterations in body weight should always be compensated by adequate alterations in food intake and thermogenesis. Thus, increased thermogenesis should not be able to counteract obesity because food intake would be increased. However evidence is presented here that thermogenesis in different forms (through artificial uncouplers, exercise, cold exposure) may counteract obesity and is not always fully compensated by increased food intake. Correspondingly, a decreased capacity for metaboloregulatory thermogenesis (i.e. non-functional brown adipose tissue) may in itself lead to obesity. This is evident in mice and may be valid for human subjects, as a substantial proportion of adults possess brown adipose tissue, and those with less or without brown adipose tissue would seem to be more prone to obesity. Thus, increased thermogenesis may counteract obesity, without dietary intervention.

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