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.

Melatonin and brown adipose tissue: novel insights to a complex interplay

2019 ◽  
Vol 2 (4) ◽  
pp. 25-41
Author(s):  
Ingrid Fernandes Olesçuck ◽  
Ludmilla Scodeler Camargo ◽  
Paula Vargas Versignassi Carvalho ◽  
Caroline Aparecida Pereira Souza ◽  
Camila Congentino Gallo ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Weight Control ◽  
Complex Interplay ◽  
Metabolic Balance ◽  
Brown Adipose ◽  
Circannual Cycles ◽  
Body Weight Control ◽  
Shivering Thermogenesis

As a chronobiotic molecule, melatonin finely tunes a variety of physiological processes including energy metabolism, reproduction and sleep-wake cycle, collaborating for the survival of the organisms. Since its pineal production occurs exclusively during the night, melatonin is responsible for signaling the circadian and circannual cycles to the organisms. This involves different ways of action that need to be considered when analyzing its effects in a given tissue/organism. Non-shivering thermogenesis (NST) is a crucial process for homeothermic animals and increasing evidences show its importance for the energy metabolic balance due to its influence in body weight control. The highly seasonal brown adipose tissue (BAT) is the site for NST and its metabolism is importantly influenced by melatonin. This review focuses on melatonin actions over BAT and the attention should be given to the relation between this signaling molecule and such a seasonally expressed tissue.

Restricted food intake limits brown adipose tissue hypertrophy in cold exposure

Life Sciences ◽  
1982 ◽  
Vol 30 (17) ◽  
pp. 1423-1426 ◽  
Author(s):  
T. Scott Johnson ◽  
Shawne Murray ◽  
James B. Young ◽  
Lewis Landsberg
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Brown Adipose ◽  
Restricted Food Intake

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.

Relationship between cold-induced thermoregulation and spontaneous rapid body weight loss of aging F344 rats

1996 ◽  
Vol 271 (5) ◽  
pp. R1115-R1122 ◽  
Author(s):  
R. B. McDonald ◽  
M. Florez-Duquet ◽  
C. Murtagh-Mark ◽  
B. A. Horwitz
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Physiological State ◽  
Rapid Weight Loss ◽  
Acute Cold Exposure ◽  
Brown Adipose ◽  
F344 Rats

We previously showed that, although cold-induced thermoregulation is attenuated in 26-mo-old male Fischer 344 (F344) rats, not all rats this age exhibit the same degree of cold-exposed hypothermia or diminished brown adipose tissue nonshivering thermogenic capacity. Examination of this heterogeneity suggested the hypothesis that it was associated with a difference in the physiological state between aged rats that were maintaining stable body weight versus those showing the rapid weight loss often occurring near the end of the rat's natural life span. To test this, we acutely exposed male F344 rats to cold (4 h at 6 degrees C) beginning at 24 mo of age. This exposure was weekly for the first 2 wk and then on alternate weeks as long as the rat's body weight was stable. If body weight progressively declined for 3-5 consecutive days, the rat's response to the acute cold exposure was again measured, as was that of two additional rats not displaying this rapid loss in body weight. If body temperature decreased during the cold exposure to intraperitoneal temperatures < or = 32.5 degrees C, the rat was killed with pentobarbital sodium and interscapular brown adipose tissue was removed. One of the age-matched controls was also killed at this time. The age at which body weight showed a spontaneous rapid decline ranged from 24.5 to 29 mos. All eight rats displaying spontaneous rapid weight loss had significant hypothermia during the acute cold exposure, whereas none of the eight weight-stable rats did. The development of hypothermia in the spontaneous rapid weight loss group was not, in general, observed before their weight loss. The weight loss and hypothermia were associated with lower levels of brown fat uncoupling protein and significant changes in body fat and protein. These data suggest that the development of senescence-related hypothermia occurs rapidly and is not a simple function of chronological age or the median life span of the animals. Furthermore, these data imply that the rate of aging in terms of maintenance of thermoregulatory homeostasis has both a gradual and rapid component, the latter being associated with a different physiological state than the former.

Insulin and metabolic efficiency in rats. II. Effects of NE and cold exposure

1986 ◽  
Vol 251 (6) ◽  
pp. R1118-R1125
Author(s):  
T. J. Bartness ◽  
C. J. Billington ◽  
A. S. Levine ◽  
J. E. Morley ◽  
N. E. Rowland ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Energy Expenditure ◽  
Cold Exposure ◽  
Diabetic Rats ◽  
Metabolic Efficiency ◽  
Maximal Energy ◽  
Brown Adipose

The role of insulin in metabolic efficiency (ME, i.e., efficiency of body wt gain) was examined under conditions of maximal energy expenditure in control and diabetic rats. Long-lasting insulin was administered using a protocol that did not affect food intake and increased ME in both groups. Half the animals were injected chronically with norepinephrine (NE). NE alone in controls decreased body weight and ME and increased brown adipose tissue (BAT) growth, thermogenic potential [cytochrome c oxidase activity (COA)], and lipoprotein lipases (LPL) activity; however, in diabetics, body weight, ME, and food intake all decreased and only BAT LPL activity and DNA content increased. The combination of NE and insulin increased BAT protein and COA in diabetics; in controls, all BAT measures were further increased and ME was intermediate to that of either treatment alone. Cold exposure decreased body weight and ME, increased food intake and qualitatively produced similar increases in BAT growth, COA, and LPL activity in both controls and diabetics. In diabetics, combined cold exposure and insulin did not affect the increase in BAT growth or LPL activity resulting from either treatment alone, but in controls this combination decreased BAT growth and COA. It is concluded that, even under conditions of maximal energy expenditure, both extremes of basal insulin status result in decreased BAT growth and thermogenic potential, but have opposite effects on ME.

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)

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