Brown Adipose Tissue: Thermic Response Increased by a Single Low Protein, High Carbohydrate Meal

Glick, Z.; Teague, R.J.; Bray, George A.

doi:10.1126/science.7268419

Cited by 93 publications

(41 citation statements)

References 22 publications

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“…Diet-induced thermogenesis is considered an obligatory energy cost for digestion, absorption, transport, and other metabolic activity needed for the assimilation of nutrients. It has also been proposed as a facultative part of adaptive thermogenesis responding to excess food intake, like nonshivering thermogensis responding to cold, that involves the sympathetic nervous system and brown adipose tissues (26)(27)(28)(29)(30). Dietary fat induces the least thermogenesis (estimated at 0 Ϫ 5%), whereas protein induces the most (20 Ϫ 30%) among the energy-yielding nutrients ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain

Nelson

Gao

Spencer

et al. 2011

Journal of Lipid Research

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for assimilation and thus exert a lower thermic effect of food (diet-induced thermogenesis) (3)(4)(5). Individuals that assimilate dietary fat effi ciently to meet their needs between meals have an advantage in enduring starvation. Thus, genes conferring this trait may be selected through evolution. During times of continuous abundance, however, individuals thrifty of energy substrates and high in metabolic effi ciency are prone to accumulating fuel surpluses in adipose and other tissues ( 6, 7 ). In humans, excessive fat accumulation is associated with metabolic diseases, including obesity, hepatic steatosis, and insulin resistance, which plague many industrialized parts of the world ( 8, 9 ).The absorption of dietary fat involves the resynthesis of digested triacylglycerol in enterocytes, mainly through a pathway catalyzed by acyl CoA:monoacylglycerol acyltransferase (MGAT) ( 10 ). Three related genes have been identifi ed that code for MGAT; among them, only Mogat2 is highly expressed in the small intestine of both mice and humans ( 11-15 ). Thus, Mogat2 probably encodes the intestinal MGAT activity, although Mogat3 is also found in the distal intestine in humans ( 14 ).Consistent with a role of MGAT2 in promoting conservation of dietary fat, mice lacking the enzyme ( Mogat2 Ϫ / Ϫ ) are resistant to obesity and other metabolic disorders induced by high-fat feeding ( 16,17 ؊ / ؊ mice expended energy and lost weight like wild-type controls. To determine whether MGAT2 defi ciency protects against obesity in the absence of high-fat feeding, we crossed Mogat2 ؊ / ؊ mice with genetically obese Agouti mice. MGAT2 defi ciency increased energy expenditure and prevented these mice from gaining excess weight. Our results suggest that MGAT2 modulates energy expenditure through multiple mechanisms, including one independent of dietary fat; these fi ndings also raise the prospect of inhibiting MGAT2 as a strategy for combating obesity and related metabolic disorders resulting from excessive calorie intake. Abbreviations: DGAT, diacylglycerol acyltransferase; MGAT, monoacylglycerol acyltransferase; RER, respiratory exchange ratio.

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Section: Discussionmentioning

confidence: 99%

Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain

Nelson

Gao

Spencer

et al. 2011

Journal of Lipid Research

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“…* P < 0.05. by guest, on May 12, 2018 www.jlr.org Downloaded from levels of key molecules involved in the regulation of mitochondrial function and thermogenesis were analyzed. The elevated energy expenditure in DBKO mice led us to fi rst study BAT, which is responsible for adaptive thermogenesis in response to diet or cold (29)(30)(31). Diet-induced thermogenesis reduces obesity in humans and animals ( 32,33 ).…”

Section: Figmentioning

confidence: 99%

Protein kinase Cβ deficiency attenuates obesity syndrome of ob/ob mice by promoting white adipose tissue remodeling

Huang

Bansode

Bal

et al. 2012

Journal of Lipid Research

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“…Nevertheless, it has to be taken into account that overfeeding leads to increased sympathetic nervous system activation and NA release from the nerve terminals innervating IBAT [17]. In these conditions, with higher levels of NA, β 3 -AR becomes more important than other ARs.…”

Section: Parametermentioning

confidence: 99%

Sexual dimorphism in the adrenergic control of rat brown adipose tissue response to overfeeding

Rodrı́guez

Monjo

Rodríguez‐Cuenca

et al. 2001

Pflügers Arch - Eur J Physiol

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Gender-related differences in the brown adipose tissue (BAT) response to overfeeding rats on a cafeteria diet were studied by assessing the balance between the expression of beta-adrenoceptors (beta1-, beta2-, beta3-AR) and alpha2A-AR and their relation to the expression of uncoupling proteins (UCP1, UCP2, UCP3). Cafeteria diet feeding for 15 days, which involved a similar degree of hyperphagia in both sexes, led to a greater body weight excess in females than in males and a lower activation of thermogenesis. Gender-related differences were found for different adrenoceptor expression and protein levels, which might explain, in part, sex differences in the thermogenic parameters. The lower expression of alpha2A-AR in females than in males could be responsible for the higher expression of UCP1 and thermogenic capacity under non-hyperphagic conditions. However, in a situation of high adrenergic stimulation--as occurs with overfeeding--as there is a preferential recruitment of the beta3-AR by noradrenaline compared with other adrenergic receptors, the higher levels of beta3-AR in males rats than in females could be responsible for the greater thermogenic capacity and the lesser weight gain in males. Thus, the alpha2/beta3 balance in BAT could be a key in the thermogenic control.

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Brown Adipose Tissue: Thermic Response Increased by a Single Low Protein, High Carbohydrate Meal

Cited by 93 publications

References 22 publications

Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain

Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain

Protein kinase Cβ deficiency attenuates obesity syndrome of ob/ob mice by promoting white adipose tissue remodeling

Sexual dimorphism in the adrenergic control of rat brown adipose tissue response to overfeeding

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