Energy balance and facultative diet-induced thermogenesis in mice fed a high-fat diet

1988 ◽  
Vol 66 (10) ◽  
pp. 1297-1302 ◽  
Author(s):  
Denis Richard ◽  
Pierre Boily ◽  
Marie-Claude Dufresne ◽  
Martin Lecompte

The present study was aimed at studying energy balance in mice fed a high-fat diet. Albino mice were divided into three groups. One group had free access to the stock diet, whereas the two other groups consumed a high-fat diet. One of the high-fat fed groups was fed ad libitum, whereas the other was offered a restricted amount of the same diet so that its energy intake was comparable to the group of mice given the stock diet. Energy balance measurements, which included indirect calorimetry and carcass analysis, were performed. Brown adipose tissue (BAT) properties were also investigated. The results show that gains in both body weight and fat were higher in mice that had free access to high-fat diet than in mice fed the stock diet. In animals given a restricted amount of the high-fat diet, fat gain increased, whereas protein gain was reduced in comparison with animals fed the stock diet. Unrestricted access to the high-fat diet led to an increase in both energy intake and energy gain. As revealed by both slaughter and indirect calorimetry techniques energy expenditure was, in high-fat fed mice, 40% higher than in animals fed either stock or a restricted amount of high-fat diet. Nadolol was shown to suppress a large part of the elevated metabolic rate seen in mice fed an unrestricted high-fat diet. In those mice, BAT mitochondrial GDP binding was also increased. In summary, the present results confirm that adaptive diet-induced thermogenesis (DIT) develops in mice made hyperphagic by an energy-dense palatable diet. The present study provides further evidence that adaptive DIT is mediated by the sympathetic nervous system and involves BAT. Finally, it appears that the extent to which adaptive DIT develops is related to the degree of hyperphagia.

2019 ◽  
Vol 121 (10) ◽  
pp. 1097-1107 ◽  
Author(s):  
Serena Boscaini ◽  
Raul Cabrera-Rubio ◽  
John R. Speakman ◽  
Paul D. Cotter ◽  
John F. Cryan ◽  
...  

AbstractRecently there has been a considerable rise in the frequency of metabolic diseases, such as obesity, due to changes in lifestyle and resultant imbalances between energy intake and expenditure. Whey proteins are considered as potentially important components of a dietary solution to the obesity problem. However, the roles of individual whey proteins in energy balance remain poorly understood. This study investigated the effects of a high-fat diet (HFD) containing α-lactalbumin (LAB), a specific whey protein, or the non-whey protein casein (CAS), on energy balance, nutrient transporters expression and enteric microbial populations. C57BL/6J mice (n 8) were given an HFD containing either 20 % CAS or LAB as protein sources or a low-fat diet containing CAS for 10 weeks. HFD-LAB-fed mice showed a significant increase in cumulative energy intake (P=0·043), without differences in body weight, energy expenditure, locomotor activity, RER or subcutaneous and epididymal white adipose tissue weight. HFD-LAB intake led to a decrease in the expression of glut2 in the ileum (P=0·05) and in the fatty acid transporter cd36 (P<0·001) in both ileum and jejunum. This suggests a reduction in absorption efficiency within the small intestine in the HFD-LAB group. DNA from faecal samples was used for 16S rRNA-based assessment of intestinal microbiota populations; the genera Lactobacillus, Parabacteroides and Bifidobacterium were present in significantly higher proportions in the HFD-LAB group. These data indicate a possible functional relationship between gut microbiota, intestinal nutrient transporters and energy balance, with no impact on weight gain.


1987 ◽  
Vol 252 (3) ◽  
pp. R617-R623 ◽  
Author(s):  
J. Arnold ◽  
D. Richard

Thermogenic response to ingestion of high-fat diet was investigated in four groups of male rats, two groups being exercise trained and two remaining sedentary. One sedentary and one trained group each received a high-fat dietary supplement in addition to the stock diet. After 35 days, body energy and protein and fat contents were determined. Results indicate that exercise reduced metabolizable energy (ME) intake by 9 and 18% in stock- and high-fat-fed trained rats, respectively. Compared with stock-fed rats, ME intake was elevated 31 and 18% in sedentary and trained high-fat-fed rats, respectively. Exercise also affected energy gains; trained rats deposited almost 60% less energy than controls. Exercise largely decreased both fat and protein contents of rats, whereas the high-fat supplement enhanced fat deposition. Energy expenditure, excluding exercise cost, was calculated on a mass-independent basis and was revealed to be similar in appropriately matched (diet) trained and sedentary rats. High-fat feeding induced increases in expenditure assumed to be due to enhanced brown adipose tissue (BAT) regulatory diet-induced thermogenesis. Conversely, exercise did not affect further the regulatory thermogenic response of BAT to stimuli originating from high-fat diet. Excluding physical activity, energy expenditure components in sum (expressed mass independently), in high-fat- and stock-fed rats, appear unaltered by exercise training.


1988 ◽  
Vol 255 (2) ◽  
pp. R226-R231
Author(s):  
Y. Deshaies ◽  
J. Arnold ◽  
J. Lalonde ◽  
D. Richard

The combined effects of a high-fat-supplemented diet and exercise training on serum lipids as well as on lipoprotein lipase activity in white and brown adipose tissues of the rat were evaluated. Male Wistar rats were fed ad libitum either a stock diet or the stock diet supplemented with food items rich in fat. Half of each dietary group was submitted to daily treadmill running for 35 days. Food intake and final body weight were raised by the high-fat-supplemented diet and lowered by exercise training. Postprandial serum triglycerides were not affected by diet or exercise, whereas the latter decreased total cholesterol in the high-fat group only (14%, P less than 0.01). Total lipoprotein lipase activity in white adipose tissue was elevated (120%, P less than 0.01) by high-fat feeding, and this increase was greatly reduced by concomitant exercise training. In brown adipose tissue, however, the large elevation (104%, P less than 0.01) in enzyme activity brought by the high-fat diet was unaltered by concomitant training. Thus a high-fat-supplemented diet increased lipoprotein lipase activity in both an energy-storing and a heat-producing tissue, and exercise training was able to counteract this effect in white, but not in brown, adipose tissue. These findings support the notion that the regulation of lipoprotein lipase is tissue specific.


1985 ◽  
Vol 249 (1) ◽  
pp. R13-R22 ◽  
Author(s):  
C. K. Smith ◽  
D. R. Romsos

Obese (ob/ob) and lean mice were adrenalectomized at 3 or 6 wk of age and fed a high-carbohydrate stock diet or a high-fat semipurified diet for 3 wk. Adrenalectomy of obese mice fed the stock diet reduced the energy intake, energy gain, and efficiency of energy retention so that the values equaled those of lean mice. Hindlimb muscle gain of adrenalectomized obese mice fed the stock diet increased by 50-100%, and concentrations of plasma insulin were reduced so that they also approached values in lean mice. In contrast to results obtained when the stock diet was fed, adrenalectomy of obese mice fed the high-fat diet resulted in only slight reductions in energy intake, energy gain, or efficiency of energy retention. Likewise, muscle gain was not improved nor were plasma insulin concentrations decreased when adrenalectomized obese mice were fed the high-fat diet. Although adrenal secretions contribute substantially to the gross obesity that develops in ob/ob mice fed the stock diet, these secretions are unnecessary for development of obesity in ob/ob mice fed the high-fat diet. Factors other than adrenal secretions per se, which are influenced by diet composition, thus mediate development of obesity in ob/ob mice.


2001 ◽  
Vol 85 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Susanna Iossa ◽  
Lillà Lionetti ◽  
Maria P. Mollica ◽  
Raffaella Crescenzo ◽  
Antonio Barletta ◽  
...  

Variations in energy balance, body composition, and nutrient partitioning induced by high-fat feeding, cold exposure or by concomitant high-fat feeding and cold exposure were studied in young Wistar rats. Changes in hepatic metabolism as well as in serum free triiodothyronine and leptin levels were also evaluated. Rats were exposed to either 24 or 4°C and fed either a low- or high-fat diet (10 % or 50 % energy respectively) for 2 weeks. Relative to low-fat feeding at 24°C, both energy intake and expenditure were increased by high-fat feeding or by cold exposure, and these changes were accompanied by increased serum triiodothyronine levels. In response to concomitant high-fat feeding and cold exposure, serum triiodothyronine tended to be further elevated, but no further increases in energy intake or energy expenditure were observed. Independently of diet, the increased energy expenditure in cold-exposed rats was not completely balanced by adaptive hyperphagia, with consequential reductions in protein and fat gain, accompanied by marked decreases in serum leptin. Furthermore, unlike high-fat feeding at 24°C, cold exposure enhanced hepatic mitochondrial oxidative capacity both in the low-fat- and high-fat-fed groups. It is concluded that in this strain of young Wistar rats, despite similarly marked stimulation of energy expenditure by high-fat feeding at 24°C, by cold exposure and by concomitant high-fat feeding and cold exposure, an increased hepatic oxidative capacity occurred only in the presence of the cold stimulus.


2021 ◽  
Vol 12 ◽  
Author(s):  
Zhuohui Luo ◽  
Jiawen Huang ◽  
Zhiping Li ◽  
Zhiwen Liu ◽  
Linchun Fu ◽  
...  

Cajanolactone A (CLA) is a stilbenoid isolated from Cajanus canjan (L.) Millsp with the potential to prevent postmenopausal obesity. In this study, the effect of CLA on high-fat diet (HFD)-induced obesity in female C57BL/6 mice was investigated. It was found that, treatment with CLA reduced the energy intake and effectively protected the mice from HFD-induced body weight gain, fat accumulation within the adipose tissues and liver, and impairment in energy metabolism. Further investigation revealed that CLA significantly down-regulated the expression of ORX, ORXR2, pMCH, and Gal in the hypothalamus and antagonized HFD-induced changes in the expression of UCP1, Pgc-1α, Tfam, and Mfn1 in the inguinal white adipose tissue (iWAT); Caveolin-1, MT and UCP3 in the perigonadal white adipose tissue (pWAT); and Pdhb, IRS2, Mttp, Hadhb, and Cpt1b in the liver. CLA also protected the pWAT and liver from HFD-induced mitochondrial damage. However, neither HFD nor CLA showed an effect on the mass of brown adipose tissue (BAT) or the expression of UCP1 in the BAT. In summary, our findings suggest that CLA is a potential drug candidate for preventing diet-induced obesity, at least in females. CLA works most likely by suppressing the hypothalamic expression of orexigenic genes, which leads to reduced energy intake, and subsequently, reduced fat accumulation, thereby protecting the adipose tissues and the liver from lipid-induced mitochondrial dysfunction.


1980 ◽  
Vol 58 (7) ◽  
pp. 842-848 ◽  
Author(s):  
Nancy J. Rothwell ◽  
Michael J. Stock

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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  

The prevalence of obesity has become a threatening global public health issue. The consequence of obesity is abnormal energy metabolism. Unlike white adipose tissue (WAT), brown adipose tissue (BAT) has a unique role in nonshivering thermogenesis. Lipids and glucose are consumed to maintain energy and metabolic homeostasis in BAT. Recently, accumulating evidence has indicated that exposure to excess maternal energy intake affects energy metabolism in offspring throughout their life. However, whether excess intrauterine energy intake influences BAT metabolism in adulthood is not clear. In this study, mouse dams were exposed to excess energy intake by feeding a high-fat diet (HFD) before and during pregnancy and lactation. The histology of BAT was assessed by hematoxylin and eosin staining. The genome-wide methylation profile of BAT was determined by a DNA methylation array, and specific site DNA methylation was quantitatively analyzed by methylated DNA immunoprecipitation (MeDIP) qPCR. We found that intrauterine exposure to a high-energy diet resulted in blood lipid panel disorders and impaired the BAT structure. Higher methylation levels of genes involved in thermogenesis and fatty acid oxidation (FAO) in BAT, such as Acaa2, Acsl1, and Cox7a1, were found in 16-week-old offspring from mothers fed with HFD. Furthermore, the expression of Acaa2, Acsl1, and Cox7a1 was down-regulated by intrauterine exposure to excess energy intake. In summary, our results reveal that excess maternal energy leads to a long-term disorder of BAT in offspring that involves the activation of DNA methylation of BAT-specific genes involved in fatty acid oxidation and thermogenesis.


1998 ◽  
Vol 275 (1) ◽  
pp. R105-R111 ◽  
Author(s):  
Konstantinia Arvaniti ◽  
Yves Deshaies ◽  
Denis Richard

The present study was conducted to assess the effects of leptin on food intake and energy balance in the presence or absence of corticosterone. Three cohorts of C57BL/6 mice differing in their corticosterone status [nonadrenalectomized (intact), adrenalectomized (ADX), and ADX with corticosterone replacement] were infused with either saline or leptin at a dose of 150 μg ⋅ kg−1 ⋅ day−1. Throughout the study, mice had free access to both a high-starch and a high-fat diet. At the end of the experimental period, mice were decapitated and their carcasses were processed for the determination of energy, protein, and lipid contents. Leptin significantly reduced body gains in weight, fat, and energy, whereas corticosterone therapy significantly promoted all of these gains. Leptin and ADX significantly reduced food intake and gross energetic efficiency, whereas corticosterone therapy significantly increased these variables. The effects of leptin, ADX, and corticosterone on food intake were accounted for by changes in the intake of the high-fat diet. Leptin also attenuated the preference for fat that developed quickly in mice simultaneously exposed to the high-starch and high-fat regimen. Altogether, the results of this study 1) emphasize the abilities of leptin and corticosterone to, respectively, decrease and increase energy deposition and ingestion of fat, 2) do not substantiate any leptin-corticosterone interaction in the regulation of energy balance, and 3) demonstrate that leptin can produce its effect on energy and fat gains in the absence of an intact hypothalamic-pituitary-adrenal axis.


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