Thermic effect of feeding carbohydrate, fat, protein and mixed meal in lean and obese subjects

Swaminathan, R.; King, R. F. G. J.; Holmfield, J. H. M.; Siwek, R A; Baker, Mary; Wales, J. K.

doi:10.1093/ajcn/42.2.177

Cited by 101 publications

(47 citation statements)

References 20 publications

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“…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 ). The lower thermic effect of fat compared with carbohydrate may explain the weight gains upon high-fat feeding ( 4,5 ). In our study, wild-type, but not Mogat2 Ϫ / Ϫ , mice have decreased postprandial metabolic rates when fed high-fat diets, suggesting that MGAT2 reduces the energy cost of fat assimilation.…”

Section: Discussionmentioning

confidence: 99%

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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%

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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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“…The modi®cations of plasma insulin and FFA levels, induced by a meal, largely in¯u-ence the subsequent patterns of substrates oxidation in normal weight subjects. We cannot exclude, however, that obese individuals (Swanimathan et al, 1985;Thomas et al, 1992) or those with a genetic predisposition to obesity (Astrup, 1993;Astrup, 1994) fail to ef®ciently utilize alimentary fat and, as a consequence, accumulate lipid in adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

Energy expenditure and substrates oxidative patterns, after glucose, fat or mixed load in normal weight subjects

et al. 1997

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Objectives: To evaluate energy balance after three isocaloric oral loads of different composition and to establish possible relationships between the substrates oxidative patterns and the modi®cations of insulin and free fatty acids (FFA) plasma pro®les. Design: Each subject received, in a randomized order, three oral loads of 2658 AE 45 kJ (636 AE 11 Kcal) either as glucose, lipids (cream) or a mixture (glucose cream). Setting: The experiments were performed at the University Hospital of Geneva. Subjects: Ten normal body-weight volunteers. Methods: Energy expenditure (EE) and substrates oxidation were measured by indirect calorimetry during 8 h following each load. Plasma glucose, insulin and FFA were also measured. Results: EE was 1776 AE 107, 1818 AE 125 and 1785 AE 117 KJ over 8 h after glucose, mixed and lipids load, respectively. Glucose oxidation was the highest after oral glucose as compared to mixed and lipids load, while the highest value of lipids oxidation was measured after fat load. A signi®cant relationship linked fat oxidation to plasma FFA (r 0.54, P`0.002) as well as to insulin (r 70.40, P`0.002). Conclusions: (a) The energetic cost of glucose and fat intake is the same; (2) after each load, the main source of energy corresponds to the substrate administered; (3) both plasma insulin and FFA in¯uence the substrate oxidative patterns observed after each load; (4) alimentary fat may contribute to fat oxidation by maintaining elevated plasma FFA levels.

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“…23 Possible explanations include underestimation of ingested quantities, decreased physical activity and reduced thermogenic response to food among overweight subjects. 24 Relative contributions of the major nutrients are not affected by the relative weight of the subjects. 23 A distinctive eating pattern among widowed and divorced men was also noted.…”

Section: Discussionmentioning

confidence: 99%

Multivariate Analysis of Dietary Patterns in 939 Swiss Adults: Sociodemographic Parameters and Alcohol Consumption Profiles

Gex‐Fabry¹,

Raymond²,

Jeanneret³

1988

Int J Epidemiol

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A dietary survey of 939 Swiss adults, randomly selected from the population of Geneva and its surrounding communities, was performed according to the history method. A factor analysis, using average weekly intake* for 33 food variables, reveals three principal components of the diet: satiating capacity, healthfulness and culinary complexity. These characteristics, together with the energy content of the diet, were analysed for differences according to sex, age, relative weight index, birthplace, marital status and occupation. Ail of these sociodemographic variables influence some dimension of dietary habits. Alcohol consumption is positively associated with satiating, protein rich diets, but energy intake from foods does not signfficatively differ between various groups of abstainers and drinkers. Although the energy contribution of alcoholic beverages is globally additive, we suggest that cultural and societal norms may modulate the relationship of alcohol and diet Food functions as a supply of energy as well as a complex behavioural code to create personal eating patterns. The energy requirement for an individual depends primarily on his basal metabolic rate, as determined by age, body size and weight, and also varies with his work-or leisure-associated level of physical activity. Additional adjustments may be needed to account for climatic variations. 1 Given these requirements and available food resources, the process of food selection depends on many factors. Physiological controls include intolerance and sensitivity to particular substances. Sensory characteristics, such as taste, visual appearance and texture, are also elements contributing to food preference or aversion. In addition, social and economic factors lead to evaluation of foods with respect to cost, convenience, prestige and healthfulness, among other criteria. 2 The influence of alcohol on diet may be considered from different points of view. It contributes to an individual's supply of energy, although the utilization of

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Thermic effect of feeding carbohydrate, fat, protein and mixed meal in lean and obese subjects

Cited by 101 publications

References 20 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

Energy expenditure and substrates oxidative patterns, after glucose, fat or mixed load in normal weight subjects

Multivariate Analysis of Dietary Patterns in 939 Swiss Adults: Sociodemographic Parameters and Alcohol Consumption Profiles

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