A high-carbohydrate diet lowers the rate of adipose tissue mitochondrial respiration

[Mito]

Abstract​

Adipocyte mitochondrial respiration may influence metabolic fuel partitioning into oxidation versus storage, with implications for whole-body energy expenditure. Although insulin has been shown to influence mitochondrial respiration, the effects of dietary macronutrient composition have not been well characterized. The aim of this exploratory study was to test the hypothesis that a high-carbohydrate diet lowers the oxygen flux of adipocyte mitochondria ex vivo. Among participants in a randomized-controlled weight-loss maintenance feeding trial, those consuming a high-carbohydrate diet (60% carbohydrate as a proportion of total energy, n = 10) had lower rates of maximal adipose tissue mitochondrial respiration than those consuming a moderate-carbohydrate diet (40%, n = 8, p = 0.039) or a low-carbohydrate diet (20%, n = 9, p = 0.005) after 10 to 15 weeks. This preliminary finding may provide a mechanism for postulated calorie-independent effects of dietary composition on energy expenditure and fat deposition, potentially through the actions of insulin on fuel partitioning.

A high-carbohydrate diet lowers the rate of adipose tissue mitochondrial respiration - European Journal of Clinical Nutrition

Adipocyte mitochondrial respiration may influence metabolic fuel partitioning into oxidation versus storage, with implications for whole-body energy expenditure. Although insulin has been shown to influence mitochondrial respiration, the effects of dietary macronutrient composition have not been...

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[Elie]

So with high carbs, adipose mitochondria are breaking down less fat? is this the idea?
i.e. less fat loss?

 

[Motorneuron]

F

 

[S.Seneff]

So with high carbs, adipose mitochondria are breaking down less fat? is this the idea?
i.e. less fat loss?

Our study suggests that a high-carbohydrate diet, possibly through an increase in insulin secretion [8], lowers mitochondrial respiratory function—a metabolic state that would favor deposition rather than oxidation of fat and predispose to weight gain. This finding is consistent with longer-term feeding trials examining the effects of dietary carbohydrate, as a proportion of total energy intake, on total energy expenditure [5], and a recent study demonstrating adverse effects of carbohydrate overfeeding on cellular redox states [10]. A mechanistic role for insulin secretion on weight gain is supported by a Mendelian randomization study, a two-cohort prospective study, and several clinical trials showing effect modification of dietary carbohydrate by insulin secretion [7, 11,12,13,14]. Nevertheless, causal roles for insulin secretion and high glycemic load diets in human obesity have not been established.

As the specific mitochondrial assays were not pre-specified, and the methods have not been standardized among laboratories (including sample storage stability), these findings should be considered preliminary. In addition, we cannot directly translate our findings to whole-body energetics. White adipose tissue is less metabolically active than lean mass, and our sample may not reflect mitochondrial activity in all body fat depots. Nevertheless, even a small shift in substrate partitioning from oxidation to storage, on the order of 1 g body fat per day, could have a major impact on obesity predisposition over the long term. Furthermore, we cannot definitively attribute the observed effects to insulin reduction per se, as other aspects of diet (e.g., fatty acid profile) or indirect influences (e.g., the microbiome) may be mechanistically involved. Additional research is needed to replicate these findings, conduct quantitative energetic studies (e.g., ATP generation), examine generalizability to other populations and experimental conditions, and explore translation to the prevention and treatment of obesity.