Thermogenesis in the marsupial Sminthopsis crassicaudata: effect of catecholamines and diet

1998 ◽  
Vol 46 (4) ◽  
pp. 381 ◽  
Author(s):  
Fiona Clements ◽  
Perdita Hope ◽  
Chris Daniels ◽  
Ian Chapman ◽  
Gary Wittert
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Food Intake ◽  
Nutritional Status ◽  
Macronutrient Composition ◽  
Sminthopsis Crassicaudata ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis ◽  
Carnivorous Marsupial ◽  
Tenebrio Molitor Larvae

The fat-tailed dunnart (Sminthopsis crassicaudata) is a small carnivorous marsupial with detectable brown adipose tissue. In order to determine whether catecholamines and food intake increase thermogenesis in this species, we measured the response of oxygen consumption (Vo2) to (i) intraperitoneal noradrenaline (0.25–4.0 mg kg-1), and (ii) food intake. The effect of nutritional status and macronutrient composition of the diet on the Vo2 response to food intake was determined by feeding both non-deprived and 24-h-food-deprived animals with either laboratory diet (1.01 Kcal g-1 (4.2 KJ g-1), 20% fat) or live mealworms (Tenebrio molitor larvae) (2.99 Kcal g-1 (12.5 KJ g-1), 30% fat). Intraperitoneal injection of noradrenaline at doses of 0.25 and 0.5 mg kg-1 increased Vo2 by 14% and 31% respectively at 30 min (P ≤ 0.05), whereas noradrenaline at 2 and 4 mg kg-1 decreased Vo2 by 10% and 31% respectively (P ≤ 0.05). Following food intake, Vo2 increased in both non-deprived (P < 0.05) and 24-h-food-deprived (P < 0.05) animals. While the magnitude of the increase in Vo2 was similar in animals fed with either laboratory diet or mealworms, both diets increased Vo2 more in non-deprived than in 24-h-food-deprived animals (P < 0.05). These results suggest that in S. crassicaudata (i) catecholamines increase thermogenesis and (ii) the magnitude of diet-induced thermogenesis is dependent on both the nutritional status of the animal and the macronutrient composition of the diet.

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.

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.

Similarities between cold- and diet-induced thermogenesis in the rat

1980 ◽  
Vol 58 (7) ◽  
pp. 842-848 ◽  
Author(s):  
Nancy J. Rothwell ◽  
Michael J. Stock
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Energy Balance ◽  
Body Temperature ◽  
Percentage Increase ◽  
Stock Diet ◽  
Interscapular Brown Adipose Tissue ◽  
The Core ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis

Rats were maintained at 24 and 4 °C (WA, CA) and fed either a pelleted stock diet (WAS, CAS) or a varied and palatable cafeteria diet (WAC, CAC). Resting oxygen consumption ([Formula: see text], 29 °C) was significantly elevated by 15, 14, and 24% in WAC, CAS, and CAC rats, respectively, compared with WAS controls and these differences were completely abolished by injection of propranolol in all but CAC rats, where [Formula: see text] remained only slightly elevated. Experimental groups showed an increased capacity to respond to the thermogenic effects of norepinephrine (percentage increase in [Formula: see text]: WAS, 43 ± 5; WAC, 88 ± 6; CAS, 75 ± 6; CAC, 128 ± 5) and greather deposits of interscapular brown adipose tissue (IBAT) (WAC, 542 ± 27; CAS, 469 ± 27; CAC, 1111 ± 85 mg) compared with WAS controls (339 ± 22 mg).When exposed to 5 °C, WAS rats shivered continuously whereas in the WAC animals shivering had ceased by 5 h. Rectal temperature was maintained at a higher level in the WAC rats than in the WAS group (WAS, 34.7 ± 0.9 °C; WAC, 36.2 ± 0.5 °C; p < 0.01). Injection of propranolol lowered the core temperature of WAC rats and caused shivering to recommence but had no effect on WAS rats.The similarities between diet- and cold-induced thermogenesis suggest that both have a common metabolic origin residing in BAT and that dietary-induced thermogenesis may be important in the maintenance of body temperature as well as in energy balance regulation.

Similar effects of NPY on energy metabolism and on plasma insulin in adrenalectomized ob/ob and lean mice

1993 ◽  
Vol 264 (2) ◽  
pp. E226-E230 ◽  
Author(s):  
H. C. Walker ◽  
D. R. Romsos
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Energy Metabolism ◽  
Food Intake ◽  
Plasma Insulin ◽  
Whole Body ◽  
Metabolic Responses ◽  
Metabolic Rates ◽  
Action Mechanisms ◽  
Brown Adipose

A single intracerebroventricular (icv) injection of dexamethasone (250 ng) lowers brown adipose tissue (BAT) thermogenesis and whole body metabolic rates and raises plasma insulin concentrations within 30 min in adrenalectomized ob/ob mice with minimal effects in adrenalectomized lean mice. The present study was conducted to determine if intracerebroventricular neuropeptide Y (NPY), a neuropeptide regulated in part by glucocorticoids, would mimic effects of dexamethasone in these mice. NPY lowered BAT metabolism and whole body oxygen consumption and raised plasma insulin concentrations within 30 min in adrenalectomized ob/ob mice similarly to dexamethasone; but, unlike dexamethasone, NPY was as effective in modulating these metabolic responses in adrenalectomized lean mice as in ob/ob mice. Further, intracerebroventricular NPY increased food intake equally in both ob/ob and lean mice, whereas dexamethasone did not alter food intake during the 30 min postinjection period. These data are consistent with the hypothesis that NPY mediates some of the effects of intracerebroventricular dexamethasone action in ob/ob mice and that the divergence between ob/ob and lean mice lies in glucocorticoid control of NPY release/synthesis rather than in NPY action mechanisms.

scholarly journals DsbA-L deficiency in T cells promotes diet-induced thermogenesis through suppressing IFN-γ production

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Haiyan Zhou ◽  
Xinyi Peng ◽  
Jie Hu ◽  
Liwen Wang ◽  
Hairong Luo ◽  
...  
Keyword(s):  
T Cells ◽  
Adipose Tissue ◽  
T Cell ◽  
Energy Homeostasis ◽  
Metabolic Diseases ◽  
Therapeutic Potential ◽  
Whole Body ◽  
Brown Adipose ◽  
Ifn Γ ◽  
Diet Induced Thermogenesis

AbstractAdipose tissue-resident T cells have been recognized as a critical regulator of thermogenesis and energy expenditure, yet the underlying mechanisms remain unclear. Here, we show that high-fat diet (HFD) feeding greatly suppresses the expression of disulfide-bond A oxidoreductase-like protein (DsbA-L), a mitochondria-localized chaperone protein, in adipose-resident T cells, which correlates with reduced T cell mitochondrial function. T cell-specific knockout of DsbA-L enhances diet-induced thermogenesis in brown adipose tissue (BAT) and protects mice from HFD-induced obesity, hepatosteatosis, and insulin resistance. Mechanistically, DsbA-L deficiency in T cells reduces IFN-γ production and activates protein kinase A by reducing phosphodiesterase-4D expression, leading to increased BAT thermogenesis. Taken together, our study uncovers a mechanism by which T cells communicate with brown adipocytes to regulate BAT thermogenesis and whole-body energy homeostasis. Our findings highlight a therapeutic potential of targeting T cells for the treatment of over nutrition-induced obesity and its associated metabolic diseases.

scholarly journals The Role of Uncoupling Protein 1 in the Metabolism and Adiposity of RIIβ-Protein Kinase A-Deficient Mice

2004 ◽  
Vol 18 (9) ◽  
pp. 2302-2311 ◽  
Author(s):  
Michael A. Nolan ◽  
Maria A. Sikorski ◽  
G. Stanley McKnight
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Uncoupling Protein ◽  
Mrna Level ◽  
Regulatory Subunit ◽  
Uncoupling Protein 1 ◽  
Brown Adipose ◽  
Kinase A

Abstract Mice lacking the RIIβ regulatory subunit of protein kinase A exhibit a 50% reduction in white adipose tissue stores compared with wild-type littermates and are resistant to diet-induced obesity. RIIβ−/− mice also have an increase in resting oxygen consumption along with a 4-fold increase in the brown adipose-specific mitochondrial uncoupling protein 1 (UCP1). In this study, we examined the basis for UCP1 induction and tested the hypothesis that the induced levels of UCP1 in RIIβ null mice are essential for the lean phenotype. The induction of UCP1 occurred at the protein but not the mRNA level and correlated with an increase in mitochondria in brown adipose tissue. Mice lacking both RIIβ and UCP1 (RIIβ−/−/Ucp1−/−) were created, and the key parameters of metabolism and body composition were studied. We discovered that RIIβ−/− mice exhibit nocturnal hyperactivity in addition to the increased oxygen consumption at rest. Disruption of UCP1 in RIIβ−/− mice reduced basal oxygen consumption but did not prevent the nocturnal hyperactivity. The double knockout animals also retained the lean phenotype of the RIIβ null mice, demonstrating that induction of UCP1 and increased resting oxygen consumption is not the cause of leanness in the RIIβ mutant mice.

CNS origins of the sympathetic nervous system outflow to brown adipose tissue

1999 ◽  
Vol 276 (6) ◽  
pp. R1569-R1578 ◽  
Author(s):  
Maryam Bamshad ◽  
C. Kay Song ◽  
Timothy J. Bartness
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Pseudorabies Virus ◽  
Critical Role ◽  
Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Diet Induced Thermogenesis

Brown adipose tissue (BAT) plays a critical role in cold- and diet-induced thermogenesis. Although BAT is densely innervated by the sympathetic nervous system (SNS), little is known about the central nervous system (CNS) origins of this innervation. The purpose of the present experiment was to determine the neuroanatomic chain of functionally connected neurons from the CNS to BAT. A transneuronal viral tract tracer, Bartha’s K strain of the pseudorabies virus (PRV), was injected into the interscapular BAT of Siberian hamsters. The animals were killed 4 and 6 days postinjection, and the infected neurons were visualized by immunocytochemistry. PRV-infected neurons were found in the spinal cord, brain stem, midbrain, and forebrain. The intensity of labeled neurons in the forebrain varied from heavy infections in the medial preoptic area and paraventricular hypothalamic nucleus to few infections in the ventromedial hypothalamic nucleus, with moderate infections in the suprachiasmatic and lateral hypothalamic nuclei. These results define the SNS outflow from the brain to BAT for the first time in any species.

scholarly journals Brown adipose tissue activity is modulated in olanzapine-treated young rats by simvastatin

2020 ◽  
Author(s):  
Xuemei Liu ◽  
Xiyu Feng ◽  
Chao Deng ◽  
Lu Liu ◽  
Yanping Zeng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Uncoupling Protein ◽  
Peroxisome Proliferator ◽  
Sprague Dawley ◽  
Olanzapine Treatment ◽  
Brown Adipose

Abstract BackgroundPrescription of second-generation antipsychotic drugs (SGAs) to childhood/adolescent has exponentially increased in recent years, which was associated with the greater risk of significant sedation, weight gain, and dyslipidemia. Statin is considered a potential preventive and treatment approach for reducing SGA-induced weight gain and dyslipidemia in schizophrenia patients. However, the effect of statin treatment in children and adolescents with SGA-induced dyslipidemia is not clearly demonstrated.MethodsTo investigate the efficacy of interventions of statin aimed at reversing SGA-induced dyslipidemia, young Sprague Dawley (SD) rats were treated orally with either olanzapine (1.0 mg/kg, t.i.d.), simvastatin (3.0 mg/kg, t.i.d.), olanzapine plus simvastatin (O+S), or vehicle (control) for 5 weeks.ResultsOlanzapine treatment increased weight gain, food intake and feeding efficiency compared to the control, while O+S co-treatment significantly reversed body weight gain but had no significant effect on food intake. Moreover, olanzapine treatment induced a slight but significant reduction in body temperature, with a decrease in locomotor activity. Fasting plasma glucose, triglycerides (TG), and total cholesterol (TC) levels were markedly elevated in the olanzapine-only group, whereas O+S co-treatment significantly ameliorated these changes. A down-regulating of uncoupling protein-1 (UCP1) and peroxisome-proliferator-activated receptor-γ co-activator-1α (PGC-1α) expression was observed in brown adipose tissue (BAT) in the olanzapine-only group, following a significant decrease in the ratio of phosphorylated PKA (p-PKA)/PKA. Interestingly, these protein changes could be reversed by co-treatment with O+B. Our results demonstrated simvastatin to be effective in ameliorating TC and TG elevated by olanzapine.ConclusionsModulation of BAT activity could be a partial mechanism in reducing metabolic side effects caused by SGAs in child and adolescent patients.

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