Relationship between insulin sensitivity and in vivo mitochondrial function in skeletal muscle

Sirikul, Bovorn; Gower, Barbara A.; Hunter, Gary R.; Larson‐Meyer, D. Enette; Newcomer, Bradley R.

doi:10.1152/ajpendo.00364.2005

Cited by 39 publications

(25 citation statements)

References 46 publications

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“…National Health and Nutrition Examination Survey [NHANES], ACLS, and HERITAGE) does appear to indicate that increased aerobic capacity among non-Hispanic Black subjects provides significant protection from adverse cardiometabolic health outcomes, namely cardiovascular disease (CVD), type 2 diabetes, and some cancers [5,17,[21][22][23]. Although there is limited, direct evidence showing that low aerobic capacity causes racial health disparities, low aerobic fitness is associated with increased heart disease risk [49]. In addition, non-Hispanic Black subjects not only have lower aerobic fitness and insulin sensitivity than non-Hispanic White subjects but lower aerobic fitness was related to lower insulin sensitivity, suggesting that aerobic fitness might be involved with increased risk of developing diabetes in non-Hispanic Black subjects [6,7,49].…”

Section: Obesity and Aerobic Capacity In African Americansmentioning

confidence: 99%

“…Although there is limited, direct evidence showing that low aerobic capacity causes racial health disparities, low aerobic fitness is associated with increased heart disease risk [49]. In addition, non-Hispanic Black subjects not only have lower aerobic fitness and insulin sensitivity than non-Hispanic White subjects but lower aerobic fitness was related to lower insulin sensitivity, suggesting that aerobic fitness might be involved with increased risk of developing diabetes in non-Hispanic Black subjects [6,7,49]. Despite the rising obesity rates among non-Hispanic Black women, and their greater risk for several cardiovascular and related diseases, negative health outcomes resulting from low aerobic capacity in this population are not well described in the literature.…”

Section: Obesity and Aerobic Capacity In African Americansmentioning

confidence: 99%

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Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes

Ceaser

Hunter

2015

Sports Med

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Obesity is a known risk factor for cardiometabolic disease. Increasing aerobic capacity (VO2max) reduces adiposity, maintains weight, and reduces the risk of developing obesity and cardiometabolic disease. Two major determinants of aerobic capacity are the metabolic properties specific to a particular muscle fiber type and the capacity of the cardiorespiratory system to deliver nutrient-rich content to the muscle. Recent research suggests that some race/ethnic groups, particularly non-Hispanic Black subjects, are predisposed to a reduced VO2max by way of muscle fiber type. Combined with insufficient physical activity, these characteristics place non-Hispanic Black subjects at an increased risk for obesity and other adverse health outcomes when compared with other race/ethnic groups. The purpose of this review was to suggest a model for explaining how skeletal muscle fiber type may contribute to reduced aerobic capacity and obesity among non-Hispanic Black subjects. Our review indicates that metabolic properties of type II skeletal muscle (e.g. reduced oxidative capacity, capillary density) are related to various cardiometabolic diseases. Based on the review, non-Hispanic Black subjects appear to have a lower maximal aerobic capacity and a greater percentage of type II skeletal muscle fibers. Combined with reduced energy expenditure and reduced hemoglobin concentration, non-Hispanic Black subjects may be inherently predisposed to a reduced maximal aerobic capacity compared with non-Hispanic White subjects, thereby increasing the risk for obesity and related metabolic diseases.

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Section: Obesity and Aerobic Capacity In African Americansmentioning

confidence: 99%

Section: Obesity and Aerobic Capacity In African Americansmentioning

confidence: 99%

Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes

Ceaser

Hunter

2015

Sports Med

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“…Furthermore, in vivo magnetic resonance spectroscopy (MRS) measurements of basal mitochondrial ATP synthesis rates (16)(17)(18) and post-exercise phosphocreatine (PCr) (19) and ADP (20) recovery kinetics also point towards a potential role for mitochondrial dysfunction in the aetiology of insulin resistance and/ or type 2 diabetes. However, it was recently shown that in vitro mitochondrial respiration of permeabilized muscle fibres from biopsies of the type 2 diabetes patients and healthy controls did not differ between groups when the data were normalized for mitochondrial DNA content or citrate synthase activity (21).…”

Section: Introductionmentioning

confidence: 99%

Early or advanced stage type 2 diabetes is not accompanied by in vivo skeletal muscle mitochondrial dysfunction

Feyter¹,

Broek²,

Praet³

et al. 2008

European Journal of Endocrinology

107

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Objective: Several lines of evidence support a potential role of skeletal muscle mitochondrial dysfunction in the pathogenesis of insulin resistance and/or type 2 diabetes. However, it remains to be established whether mitochondrial dysfunction represents either cause or consequence of the disease. We examined in vivo skeletal muscle mitochondrial function in early and advanced stages of type 2 diabetes, with the aim to gain insight in the proposed role of mitochondrial dysfunction in the aetiology of insulin resistance and/or type 2 diabetes. Methods: Ten long-standing, insulin-treated type 2 diabetes patients, 11 subjects with impaired fasting glucose, impaired glucose tolerance and/or recently diagnosed type 2 diabetes, and 12 healthy, normoglycaemic controls, matched for age and body composition and with low habitual physical activity levels were studied. In vivo mitochondrial function of the vastus lateralis muscle was evaluated from post-exercise phosphocreatine (PCr) recovery kinetics using 31 P magnetic resonance spectroscopy (MRS). Intramyocellular lipid (IMCL) content was assessed in the same muscle using single-voxel 1 H MRS. Results: IMCL content tended to be higher in the type 2 diabetes patients when compared with normoglycaemic controls (PZ0.06). The 31 P MRS parameters for mitochondrial function, i.e. PCr and ADP recovery time constants and maximum aerobic capacity, did not differ between groups. Conclusions: The finding that in vivo skeletal muscle oxidative capacity does not differ between longstanding, insulin-treated type 2 diabetes patients, subjects with early stage type 2 diabetes and sedentary, normoglycaemic controls suggests that mitochondrial dysfunction does not necessarily represent either cause or consequence of insulin resistance and/or type 2 diabetes.European Journal of Endocrinology 158 643-653

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“…Overweight African-American (AA) women are more hyperinsulinemic and resistant to insulin's glucoregulatory actions than body fat-matched Caucasian (C) women ( 5,6 ). Thus, it is logical to postulate that AAs may also exhibit higher rates of lipolysis and resistance to the antilipolytic effect of insulin.…”

mentioning

confidence: 99%

Resistance to the antilipolytic effect of insulin in adipocytes of African-American compared to Caucasian postmenopausal women

Fried

Tittelbach²,

Blumenthal³

et al. 2010

Journal of Lipid Research

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Increased availability of nonesterifi ed fatty acids (FA) contributes to the metabolic dysfunction associated with obesity, including systemic insulin resistance and hyperlipidemia ( 1 ). It is well established that central or upper body obesity, independent of total body fat, is associated with elevated systemic nonesterifi ed FA turnover in premenopausal women. In vivo studies of FA fl uxes show that on a per gram basis, abdominal (Abd) subcutaneous (sc) fat is the main source of the high systemic lipolysis in upper body compared with lower body obese premenopausal women and that leg fat is less lipolytically active ( 1 ). However, microdialysis studies detect no depot difference in lipolysis in nonobese, premenopausal Abd and femoral sc adipose tissue ( 2 ). Nevertheless, both techniques reveal similar responses to the antilipolytic effect of insulin in Abd sc and lower body adipose tissues. In vitro studies also show similar basal lipolytic rates in Abd and gluteal (Glt) or femoral adipocytes of premenopausal women, but Glt adipocytes are more sensitive to insulin ( 3, 4 ). Whether this depot difference exists in postmenopausal women is not known, so this was one of the objectives of the current study.Overweight African-American (AA) women are more hyperinsulinemic and resistant to insulin's glucoregulatory actions than body fat-matched Caucasian (C) women ( 5, 6 ). Thus, it is logical to postulate that AAs may also exhibit higher rates of lipolysis and resistance to the antilipolytic effect of insulin. However, results in the literature on this topic are inconsistent. In premenopausal women, Abstract High fatty acid (FA) fl ux is associated with systemic insulin resistance, and African-American (AA) women tend to be more insulin resistant. We assessed possible depot and race difference in the antilipolytic effect of insulin in adipocytes isolated from abdominal (Abd) and gluteal (Glt) subcutaneous (sc) adipose tissue of overweight, postmenopausal AA and Caucasian (C) women. Percent body fat, fasting insulin, visceral adiposity, and adipocyte size was higher in AA women. Disinhibited lipolysis (presence of adenosine deaminase) per unit adipocyte surface area was similar in Abd and Glt and in AA and C. However, rates of 'basal' [submaximal phenylisopropyl adenosine (PIA) -suppressed] and insulin-suppressed lipolysis were higher in Abd of AA compared with C women even after adjustment for percent fat and visceral fat area. The race difference in rates of PIA-and insulin-suppressed lipolysis in AA were correlated with their hyperinsulinemia, but AA race, independent of fasting insulin, was associated with lower responsiveness (percent suppression) to submaximal insulin concentrations, although sensitivity (ED50) was not affected. Overall, these data are consistent with the hypothesis that decreased responsiveness of Abd adipocytes to antilipolytic effectors may contribute to higher FA availability and thereby to racial differences in insulin resistance. -Fried,

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Relationship between insulin sensitivity and in vivo mitochondrial function in skeletal muscle

Cited by 39 publications

References 46 publications

Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes

Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes

Early or advanced stage type 2 diabetes is not accompanied by in vivo skeletal muscle mitochondrial dysfunction

Resistance to the antilipolytic effect of insulin in adipocytes of African-American compared to Caucasian postmenopausal women

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