scholarly journals Racial Differences In Peripheral Insulin Sensitivity and Mitochondrial Capacity in the Absence of Obesity

2014 ◽  
Vol 99 (11) ◽  
pp. 4307-4314 ◽  
Author(s):  
James P. DeLany ◽  
John J. Dubé ◽  
Robert A. Standley ◽  
Giovanna Distefano ◽  
Bret H. Goodpaster ◽  
...  
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Oxidative Capacity ◽  
Hepatic Insulin Sensitivity ◽  
Peripheral Insulin Sensitivity ◽  
Mitochondrial Oxidative Capacity ◽  
Mitochondrial Capacity

Context: African-American women (AAW) have an increased risk of developing type 2 diabetes compared with Caucasian women (CW). Lower insulin sensitivity has been reported in AAW, but the reasons for this racial difference and the contributions of liver versus skeletal muscle are incompletely understood. Objective: We tested the hypothesis that young, nonobese AAW manifest lower insulin sensitivity specific to skeletal muscle, not liver, and is accompanied by lower skeletal muscle mitochondrial oxidative capacity. Participants and Main Outcome Measures: Twenty-two nonobese (body mass index 22.7 ± 3.1 kg/m2) AAW and 22 matched CW (body mass index 22.7 ± 3.1 kg/m2) underwent characterization of body composition, objectively assessed habitual physical activity, and insulin sensitivity with euglycemic clamps and stable-isotope tracers. Skeletal muscle biopsies were performed for lipid content, fiber typing, and mitochondrial measurements. Results: Peripheral insulin sensitivity was 26% lower in AAW (P < .01), but hepatic insulin sensitivity was similar between groups. Physical activity levels were similar between groups. Lower insulin sensitivity in AAW was not explained by total or central adiposity. Skeletal muscle triglyceride content was similar, but mitochondrial content was lower in AAW. Mitochondrial respiration was 24% lower in AAW and correlated with skeletal muscle insulin sensitivity (r = 0.33, P < .05). Conclusion: When compared with CW, AAW have similar hepatic insulin sensitivity but a muscle phenotype characterized by both lower insulin sensitivity and lower mitochondrial oxidative capacity. These observations occur in the absence of obesity and are not explained by physical activity. The only factor associated with lower insulin sensitivity in AAW was mitochondrial oxidative capacity. Because exercise training improves both mitochondrial capacity and insulin sensitivity, we suggest that it may be of particular benefit as a strategy for diabetes prevention in AAW.

Associations Among Physical Activity Level and Skeletal Muscle Antioxidants in Older Adults

2020 ◽  
Vol 17 (9) ◽  
pp. 895-901
Author(s):  
Kyle L. Timmerman ◽  
Kevin D. Ballard ◽  
Michael A. Deal ◽  
Lisa C. Tagariello ◽  
Jenna M. Karrow ◽  
...  
Keyword(s):  
Physical Activity ◽  
Older Adults ◽  
Skeletal Muscle ◽  
Body Mass Index ◽  
Glutathione Peroxidase ◽  
Body Mass ◽  
Oxidized Ldl ◽  
Maximal Oxygen Consumption ◽  
Glutathione Peroxidase 1 ◽  
Endogenous Antioxidants

Background: Endogenous antioxidants are critical to limiting cellular oxidative damage. Methods: The authors determined if habitual physical activity (PA) and cardiorespiratory fitness were associated with skeletal muscle expression of endogenous antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) and circulating oxidative stress markers (serum 8-hydroxy-2′-deoxyguanosine [8-OHdG]; oxidized low-density lipoprotein [LDL]) in older adults. Moderate to vigorous PA (MVPA) was estimated using a validated PA questionnaire in 26 older adults (mean [SD]; M/F = 9/17, age = 68 [4] y, body mass index = 26 [3] kg·m−2). Maximal oxygen consumption was estimated using the YMCA submaximal cycle test. Skeletal muscle endogenous antioxidants and serum 8-OHdG and oxidized LDL were measured. Bivariate and partial correlations (controlling for body mass index) were utilized to determine associations among variables. Results: MVPA (1640 [1176] kcal·wk−1) was correlated with superoxide dismutase 2 (r = .55), catalase (r = .55), glutathione peroxidase 1 (r = .48), and 8-OHdG (r = −.41) (all Ps < .05), but not oxidized LDL. MVPA and 8-OHdG were not significantly correlated when controlling for body mass index (r = −.29). Estimated maximal oxygen consumption was correlated with glutathione peroxidase 1 (r = .48; P < .05). Conclusions: These data show that skeletal muscle endogenous antioxidant expression and circulating oxidative damage are associated with habitual MVPA in older adults. Thus, MVPA in older adults may be protective against reactive oxygen species damage due to higher expression of endogenous antioxidants.

scholarly journals Impact of aging and exercise on skeletal muscle mitochondrial capacity, energy metabolism, and physical function

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
L. Grevendonk ◽  
N. J. Connell ◽  
C. McCrum ◽  
C. E. Fealy ◽  
L. Bilet ◽  
...  
Keyword(s):  
Physical Activity ◽  
Older Adults ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Mitochondrial Function ◽  
Physical Activity Level ◽  
Activity Level ◽  
Muscle Physiology ◽  
Activity Levels ◽  
Mitochondrial Capacity

AbstractThe relationship between the age-associated decline in mitochondrial function and its effect on skeletal muscle physiology and function remain unclear. In the current study, we examined to what extent physical activity contributes to the decline in mitochondrial function and muscle health during aging and compared mitochondrial function in young and older adults, with similar habitual physical activity levels. We also studied exercise-trained older adults and physically impaired older adults. Aging was associated with a decline in mitochondrial capacity, exercise capacity and efficiency, gait stability, muscle function, and insulin sensitivity, even when maintaining an adequate daily physical activity level. Our data also suggest that a further increase in physical activity level, achieved through regular exercise training, can largely negate the effects of aging. Finally, mitochondrial capacity correlated with exercise efficiency and insulin sensitivity. Together, our data support a link between mitochondrial function and age-associated deterioration of skeletal muscle.

scholarly journals Obesity, insulin resistance, and skeletal muscle nitric oxide synthase

2012 ◽  
Vol 113 (5) ◽  
pp. 758-765 ◽  
Author(s):  
Raymond M. Kraus ◽  
Joseph A. Houmard ◽  
William E. Kraus ◽  
Charles J. Tanner ◽  
Joseph R. Pierce ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Nitric Oxide Synthase ◽  
Body Mass ◽  
Inos Protein ◽  
Oxide Synthase ◽  
Nonobese Group

The molecular mechanisms responsible for impaired insulin action have yet to be fully identified. Rodent models demonstrate a strong relationship between insulin resistance and an elevation in skeletal muscle inducible nitric oxide synthase (iNOS) expression; the purpose of this investigation was to explore this potential relationship in humans. Sedentary men and women were recruited to participate (means ± SE: nonobese, body mass index = 25.5 ± 0.3 kg/m2, n = 13; obese, body mass index = 36.6 ± 0.4 kg/m2, n = 14). Insulin sensitivity was measured using an intravenous glucose tolerance test with the subsequent modeling of an insulin sensitivity index (SI). Skeletal muscle was obtained from the vastus lateralis, and iNOS, endothelial nitric oxide synthase (eNOS), and neuronal nitric oxide synthase (nNOS) content were determined by Western blot. SI was significantly lower in the obese compared with the nonobese group (∼43%; P < 0.05), yet skeletal muscle iNOS protein expression was not different between nonobese and obese groups. Skeletal muscle eNOS protein was significantly higher in the nonobese than the obese group, and skeletal muscle nNOS protein tended to be higher ( P = 0.054) in the obese compared with the nonobese group. Alternative analysis based on SI (high and low tertile) indicated that the most insulin-resistant group did not have significantly more skeletal muscle iNOS protein than the most insulin-sensitive group. In conclusion, human insulin resistance does not appear to be associated with an elevation in skeletal muscle iNOS protein in middle-aged individuals under fasting conditions.

Abstract P261: Performing Recommended Physical Activity and Insulin Sensitivity by Body Mass Index, among US Adolescents: NHANES 1999–2006

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
MinKyoung Song ◽  
Dianna D Carroll ◽  
Giuseppina Imperatore ◽  
Carl J Caspersen ◽  
Janet E Fulton
Keyword(s):  
Physical Activity ◽  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Weight Status ◽  
Weight Lifting ◽  
Intensity Level ◽  
Significant Positive Association ◽  
Muscle Strengthening ◽  
Enhance Insulin Sensitivity

Introduction: Physical activity may enhance insulin sensitivity in youth, thereby reducing future risk of type 2 diabetes. However, no studies report the association between performing aerobic- or muscle-strengthening (MS) activities recommended in the 2008 Physical Activity Guidelines for Americans and insulin sensitivity, especially by body mass index (BMI) levels. Objective: To assess the association between meeting aerobic or muscle-strengthening guidelines and insulin sensitivity overall, and by BMI levels, in a nationally representative sample of US adolescents. Methods: We analyzed National Health and Nutrition Examination Survey (1999–2006) data for 2251 adolescents aged 12–17 years who answered 10 interviewer-administered physical activity questions. Adolescents met the aerobic guideline with ≥60 minutes/day of moderate- or vigorous- intensity level aerobic activities, and the MS guideline with ≥3 days/week of activities such as weight lifting or push-ups. We estimated insulin sensitivity via the Quantitative Insulin Sensitivity Check Index (QUICKI) calculated as 100/[log fasting insulin (μ U/mL) + log fasting plasma glucose (mg/dl)]. We used multivariable linear regression to assess the association between meeting the aerobic or MS guideline and insulin sensitivity overall, and by BMI levels (<85, 85–94, and ≥95 percentile), adjusting for demographics (age, sex, race/ethnicity, and family poverty income ratio). Significance was set at p < 0.05. Results: For these US adolescents, 40.6% [95% confidence interval (CI), 37.2, 44.1] met the aerobic guideline, 37.5% [34.2, 40.9] met the MS guideline, and their mean QUICKI value was 35.0 [34.7, 35.3]. With no adjustments, we found significantly higher insulin sensitivity values for meeting the aerobic guideline (ß=0.43 [0.04, 0.83]) and the MS guideline (ß=0.70 [0.24, 1.16]). After adjusting for demographics and meeting the aerobic guideline, adolescents meeting the MS guideline still had significantly higher levels of insulin sensitivity (ß=0.58 [0.08, 1.08]) which remained significant only for obese adolescents (BMI ≥95 percentile) (ß=0.87 [0.30, 1.45]) when stratified on weight status. With similar adjustments including meeting the MS guideline, those meeting the aerobic guideline did not have significantly higher QUICKI values. Conclusions: We found a significant positive association between meeting the MS guideline and insulin sensitivity among US adolescents who are obese. Increasing participation in MS activities might viably enhance insulin sensitivity among obese US adolescents to reduce future diabetes risk.

Skeletal muscle mitochondria exhibit decreased pyruvate oxidation capacity and increased ROS emission during surgery-induced acute insulin resistance

2015 ◽  
Vol 308 (8) ◽  
pp. E613-E620 ◽  
Author(s):  
Martin Hagve ◽  
Petter Fosse Gjessing ◽  
Ole Martin Fuskevåg ◽  
Terje S. Larsen ◽  
Øivind Irtun
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Mitochondrial Function ◽  
Enzyme Activities ◽  
Surgical Trauma ◽  
Hepatic Insulin Sensitivity ◽  
Oxidation Capacity ◽  
Peripheral Insulin Sensitivity ◽  
Pyruvate Oxidation

Development of acute insulin resistance represents a negative factor after surgery, but the underlying mechanisms are not fully understood. We investigated the postoperative changes in insulin sensitivity, mitochondrial function, enzyme activities, and release of reactive oxygen species (ROS) in skeletal muscle and liver in pigs on the 2nd postoperative day after major abdominal surgery. Peripheral and hepatic insulin sensitivity were assessed by d-[6,6-2H2]glucose infusion and hyperinsulinemic euglycemic step clamping. Surgical trauma elicited a decline in peripheral insulin sensitivity (∼34%, P < 0.01), whereas hepatic insulin sensitivity remained unchanged. Intramyofibrillar (IFM) and subsarcolemma mitochondria (SSM) isolated from skeletal muscle showed a postoperative decline in ADP-stimulated respiration (VADP) for pyruvate (∼61%, P < 0.05, and ∼40%, P < 0.001, respectively), whereas VADP for glutamate and palmitoyl-l-carnitine (PC) was unchanged. Mitochondrial leak respiration with PC was increased in SSM (1.9-fold, P < 0.05) and IFM (2.5-fold, P < 0.05), indicating FFA-induced uncoupling. The activity of the pyruvate dehydrogenase complex (PDC) was reduced (∼32%, P < 0.01) and positively correlated to the decline in peripheral insulin sensitivity ( r = 0.748, P < 0.05). All other mitochondrial enzyme activities were unchanged. No changes in mitochondrial function in liver were observed. Mitochondrial H2O2 and O2·− emission was measured spectrofluorometrically, and H2O2 was increased in SSM, IFM, and liver mitochondria (∼2.3-, ∼2.5-, and ∼2.3-fold, respectively, all P < 0.05). We conclude that an impairment in skeletal muscle mitochondrial PDC activity and pyruvate oxidation capacity arises in the postoperative phase along with increased ROS emission, suggesting a link between mitochondrial function and development of acute postoperative insulin resistance.

Neuregulins Increase Mitochondrial Oxidative Capacity and Insulin Sensitivity in Skeletal Muscle Cells

Diabetes ◽  
2007 ◽  
Vol 56 (9) ◽  
pp. 2185-2193 ◽  
Author(s):  
C. Canto ◽  
S. Pich ◽  
J. C. Paz ◽  
R. Sanches ◽  
V. Martinez ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Muscle Cells ◽  
Oxidative Capacity ◽  
Skeletal Muscle Cells ◽  
Mitochondrial Oxidative Capacity

scholarly journals Insulin-Like Growth Factor Binding Protein 1 as a Novel Specific Marker of Hepatic Insulin Sensitivity

2008 ◽  
Vol 93 (12) ◽  
pp. 4867-4872 ◽  
Author(s):  
Anna Kotronen ◽  
Moira Lewitt ◽  
Kerstin Hall ◽  
Kerstin Brismar ◽  
Hannele Yki-Järvinen
Keyword(s):  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Binding Protein ◽  
Fat Content ◽  
Liver Fat ◽  
Specific Marker ◽  
Liver Fat Content ◽  
C Peptide ◽  
Hepatic Insulin Sensitivity

Background and Aims: The liver is the main source and insulin the main regulator of IGF binding protein 1 (IGFBP-1) in humans. Here we examined how serum IGFBP-1 concentrations are related to directly measured hepatic insulin sensitivity and liver fat content in humans. Methods: We measured fasting serum (fS) IGFBP-1 concentrations and liver fat content by proton magnetic resonance spectroscopy in 113 nondiabetic subjects. In addition, hepatic insulin sensitivity was measured using the euglycemic hyperinsulinemic clamp (insulin 0.3 mU/kg·min) technique in combination with the infusion of [3-(3)H]glucose in 78 subjects. Results: fS-IGFBP-1 concentrations were inversely related to liver fat content (r = −0.38, P &lt; 0.0001). Of circulating parameters, fS-IGFBP-1 was better correlated to hepatic insulin sensitivity (r = 0.48, P &lt; 0.0001) than fS-insulin (r = −0.42, P = 0.0001), fS-C-peptide (r = −0.41, P = 0.0002), fS-triglyceride (r = −0.33, P = 0.003), or fS-high-density lipoprotein cholesterol (r = 0.30, P = 0.007). In multiple linear regression analyses, body mass index (P &lt; 0.0001) and fS-IGFBP-1 (P = 0.008), but neither age nor gender, were independently associated with hepatic insulin sensitivity (P &lt; 0.0001 for ANOVA). Neither fS-insulin nor fS-C-peptide were independent determinants of hepatic insulin sensitivity after adjusting for age, gender, and body mass index. Conclusions: fS-IGFBP-1 is inversely correlated with liver fat and is an obesity-independent and liver-specific circulating marker of hepatic insulin sensitivity.

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