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Background and Aims: Ectopic lipid storage is implicated in type 2 diabetes pathogenesis; hence, exercise to deplete stores (i.e., at the intensity that allows for maximal rate of lipid oxidation; MLO) might be optimal for restoring metabolic health. This intensity ("Fat max ") is estimated during incremental exercise ("Fat max test"). However, in "the field" general recommendations exist regarding a range of percentages of maximal heart rate (HR) to elicit MLO. The degree to which this range is aligned with measured Fat max has not been investigated. We compared measured HR at Fat max , with maximal HR percentages within the typically recommended range in a sample of 26 individuals (Female: n = 11, European ancestry: n = 17)., Methods and Results: Subjects completed a modified Fat max test with a 5-min warmup, followed by incremental stages starting at 15 W with work rate increased by 15 W every 5 min until termination criteria were reached. Pulmonary gas exchange was recorded and average values for V˙ o 2 and V˙ co 2 for the final minute of each stage were used to estimate substrate-oxidation rates. We modeled lipid-oxidation kinetics using a sinusoidal model and expressed MLO relative to peak V˙ o 2 and HR. Bland-Altman analysis demonstrated lack of concordance between HR at Fat max and at 50%, 70%, and 80% of age-predicted maximum with a mean difference of 23 b·min -1 ., Conclusion: Our results indicate that estimated "fat-burning" heart rate zones are inappropriate for prescribing exercise to elicit MLO and we recommend direct individual exercise lipid oxidation measurements to elicit these values., Competing Interests: Declaration of competing interest No conflicts of interest, financial or otherwise, are declared by the authors., (Copyright © 2023 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

Background: Epidemiologic evidence has shown a link between short sleep and obesity. Clinical studies suggest a role of increased energy intake in this relation, whereas the contributions of energy expenditure (EE) and substrate utilization are less clearly defined., Objective: Our aim was to investigate the effects of sleep curtailment on 24-h EE and respiratory quotient (RQ) by using whole-room indirect calorimetry under fixed-meal conditions., Design: Ten females aged 22-43 y with a BMI (in kg/m²) of 23.4-27.5 completed a randomized, crossover study. Participants were studied under short- (4 h/night) and habitual- (8 h/night) sleep conditions for 3 d, with a 4-wk washout period between visits. Standardized weight-maintenance meals were served at 0800, 1200, and 1900 with a snack at 1600. Measures included EE and RQ during the sleep episode on day 2 and continuously over 23 h on day 3., Results: Short compared with habitual sleep resulted in significantly higher (± SEM) 24-h EE (1914.0 ± 62.4 compared with 1822.1 ± 43.8 kcal; P = 0.012). EE during the scheduled sleep episode (0100-0500 and 2300-0700 in short- and habitual-sleep conditions, respectively) and across the waking episode (0800-2300) were unaffected by sleep restriction. RQ was unaffected by sleep restriction., Conclusions: Short compared with habitual sleep is associated with an increased 24-h EE of ~92 kcal (~5%)--lower than the increased energy intake observed in prior sleep-curtailment studies. This finding supports the hypothesis that short sleep may predispose to weight gain as a result of an increase in energy intake that is beyond the modest energy costs associated with prolonged nocturnal wakefulness.

Purpose: Epidemiologic studies suggest that insulin-like growth factor-1 (IGF-1) is associated with obesity and, more recently, cancer. This study investigates multiple lifestyle, physiologic, and anthropometric determinants of circulating IGF-1 concentrations., Methods: Nationally representative data were used from the cross-sectional Third National Health and Nutrition Examination (NHANES III, 1988-1994) survey, which measured IGF-1 concentrations in blood, from a subsample of participants who were examined in the morning. After exclusion of persons with missing data, 6,058 men and women 20 years of age or older were included in the study., Results: The mean IGF-1 concentrations were 260 ng/mL in the entire population and were higher among men as compared with women (278.8 vs. 241.3 ng/mL; p<0.0001). IGF-1 decreased with increasing age (p<0.0001), body mass index (p<0.0001), and waist circumference (p<0.0001). Individuals with metabolic syndrome had lower IGF-1 concentrations after adjustment for covariates (p=0.0008). IGF-1 was inversely associated with increasing number of metabolic syndrome abnormalities (p=0.0008). All associations were stronger among women compared with men except across concentrations of glucose. IGF-1 concentrations did not vary by any other lifestyle or physiologic factors., Conclusions: Age, adiposity, hyperglycemia, and metabolic syndrome influenced circulating IGF-1 concentrations. Diet and physical activity had no impact on IGF-1 in this nationally representative population., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)

We measured gene expression of paracrine regulators involved in adipocyte differentiation within the stromovascular fraction of abdominal subcutaneous adipose tissue from obese individuals with (n=30) and without (n=18) type 2 diabetes mellitus (T2DM). Despite similar adiposity by design, subjects with T2DM had larger adipocytes (0.92+/-0.28 vs. 0.75+/-0.17 microl, p<0.05) than controls. Gene expression of the adipogenic marker aP2 was lower (0.35+/-0.16 vs. 0.58+/-0.27 arbitrary units, p<0.05) whereas the expression of matricellular peptidase, MMP2 was higher (1.65+/-0.17 vs. 1.27+/-0.21, p=0.02) in T2DM vs. controls. The gene expression levels between the aP2 and MMP2 were inversely correlated (r=-0.32, p=0.03). We conclude that early steps of adipogenesis may be impaired in T2DM independently of obesity due, in part, to an upregulation of the MMP2 transcription.

Background: Obesity and insulin resistance are growing problems in HIV-positive (HIV+) women receiving highly active antiretroviral therapy (HAART)., Objective: The objective was to determine the contribution of adipose tissue (AT) enlargement and distribution to the presence of insulin resistance in obese HIV+ women., Design: Whole-body intermuscular AT (IMAT), visceral AT (VAT), subcutaneous AT (SAT), and SAT distribution (leg versus upper body) were measured by whole-body magnetic resonance imaging. Insulin sensitivity (S(I)) was measured with an intravenous glucose tolerance test in obese HIV+ women recruited because of their desire to lose weight (n=17) and in obese healthy controls (n=32)., Results: The HIV+ women had relatively less whole-body SAT and more VAT and IMAT than did the controls (P<0.05 for all). A significant interaction by HIV status was observed for the relation of total SAT with S(I) (P<0.001 for the regression's slope interactions after adjustment for age, height, and weight). However, relations of IMAT, VAT, and SAT distribution (leg SAT as a percentage of total SAT; leg SAT%) with S(I) did not differ significantly between groups. For both groups combined, the best model predicting a low S(I) included significant contributions by both high IMAT and low leg SAT%, independent of age, height, and weight, and no interaction between groups was observed (overall r(2)=0.44, P=0.0003)., Conclusion: In obese HIV+ women, high whole-body IMAT and low leg SAT% distribution are independently associated with insulin resistance.

Background: African Americans (AAs) have a higher prevalence of obesity and type 2 diabetes than do whites. Higher insulin resistance and hyperinsulinemia have been reported in adult AAs than in whites. Differences in adipose tissue and its distribution may account for these findings., Objective: The objective was to ascertain whether differences between AA and white women in adipose tissue (AT) and skeletal muscle (SM) volumes account for ethnic differences in insulin resistance., Design: We used whole-body magnetic resonance imaging to measure AT and SM volumes and used the intravenous-glucose-tolerance test to measure insulin resistance., Results: AAs (n = 32) were 29-42% more insulin resistant than were whites (n = 28) after adjustment for weight and height or any AT volumes (P < 0.05). After adjustment for SM volume, the difference decreased to 19% and became nonsignificant. AAs had a 163% greater acute insulin response to glucose than did whites; this difference was significant even after adjustment for insulin sensivitity index, weight, height, and any magnetic resonance imaging measures. With respect to regional AT volumes, an association independent of race, weight, height, and SM volume was found only between increased intermuscular AT and lower insulin sensitivity index., Conclusions: Premenopausal AA women had significantly higher insulin resistance and acute insulin response to glucose than did their white counterparts. Whereas the difference in insulin resistance was partially accounted for by a greater SM volume in the AAs than in the whites, the difference in the acute insulin response to glucose was independent of any AT and SM measures and was disproportionately larger than expected according to the difference in insulin resistance. In addition, whole-body intermuscular AT was an important independent correlate of insulin resistance.