Abstract
BackgroundMetabolic flexibility described as “the capacity of the body to match fuel oxidation to fuel availability” has been implicated in insulin resistance. We examined fasting substrate oxidation in relation to dietary macronutrient intake, and markers of insulin resistance in otherwise healthy women, with and without a family history of diabetes mellitus (FH DM).MethodsWe measured body composition (dual x-ray absorptiometry), visceral and subcutaneous adipose tissue area (VAT, SAT, using Computerised Tomography), fasting [glucose], [insulin], [free fatty acids], [blood lipids], insulin resistance (HOMA-IR), resting energy expenditure (REE), respiratory exchange ratio(RER) and self-reported physical activity in a convenience sample of 180 women (18-45 yrs). A food frequency questionnaire was used to assess energy intake (EI) and calculate the RER: Food Quotient (FQ) ratio. Only those with EI:REE (1.05 -2.28) were included (N=140). Insulin resistance was defined HOMA-IR (>1.95).ResultsThe Insulin Resistant (IR) group had higher energy, carbohydrate and protein intakes (p < 0.05) and lower PA levels than Insulin Sensitive (IS) group (P < 0.001), but there were no differences in RER or RER:FQ between groups. However, nearly 50% of the variance in HOMA-IR was explained by age, body fat %, VAT, RER:FQ and FH DM (adjusted R2 = 0.50, p < 0.0001). Insulin-resistant women, and those with FH DM had a higher RER:FQ than their counterparts (p < 0.01), independent of body fat % or distribution.ConclusionIn these apparently healthy, weight-stable women, insulin resistance and FH DM were associated with lower fat oxidation in relation to dietary fat intake, suggesting lower metabolic flexibility.
Highlights
Metabolic flexibility described as “the capacity of the body to match fuel oxidation to fuel availability” has been implicated in insulin resistance
Factors associated with substrate oxidation (RER), insulin resistance (HOMA-Insulin Resistant (IR)) and metabolic flexibility (RER:Food Quotient (FQ)) When combining the groups (Table 4), we showed that certain lifestyle variables and body composition were associated with HOMA-IR
The link between substrate oxidation or metabolic flexibility and family membership, as well as, family history of diabetes, has been demonstrated using 24-hr resting energy expenditure [14,30], fasting substrate oxidation [34] and suppression of fat oxidation in response to insulin-induced glycaemia and in response to high-fat feeding, Ukropcova [17,19], hypothesized that patterns of fat oxidation are genetically or epigenetically determined, in that, the differences in metabolic phenotype were independent of body fat percentage
Summary
Metabolic flexibility described as “the capacity of the body to match fuel oxidation to fuel availability” has been implicated in insulin resistance. Obesity and diabetes have become major public health problems in both developed and developing countries [2,3,4]. This trend in obesity may be linked to changes in population levels of physical activity [5], along with a changing food. The link between fat intake and overweight is not limited to the high-energy content of fatty foods, but has been shown to be associated with a reduced capacity to oxidize dietary fat [11,12,13,14]. Metabolic flexibility as an ‘intrinsic property of skeletal muscle’ has been further supported by in vitro studies in which the capacity of glucose to suppress fat oxidation in cultured myotubes from muscle biopsy samples was inversely correlated with in vivo insulin sensitivity and positively correlated to % body fat and serum free fatty acid levels [17]
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