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Steen B Haugaard, Huiling Mu, Allan Vaag and Sten Madsbad


It remains unknown whether sex impacts on intramyocellular triglyceride (IMTG) in obesity, as has been shown in non-obese subjects, and, if so, whether this may have implications on the association between IMTG and insulin sensitivity.

Subject and methods

A muscle biopsy from vastus lateralis was obtained in 27 obese women (body mass index (BMI)=35.5±0.8 kg/m2; mean±s.e.m., percentage of body fat (PBF)=44±1, n=7  impaired fasting glucose, n=7 type 2 diabetes), 20 obese men (BMI=35.8±0.8 kg/m2; PBF=33±1, n=4 impaired-fasting-glucose; n=6 type 2 diabetes) and 12 lean sedentary healthy individuals (controls; n=7 women, BMI=21.8±0.7 kg/m2, PBF=20±2; n=5 men, BMI=23.6±0.5 kg/m2, PBF=13±2). IMTG was determined by chromatography.


IMTG was increased twofold in obese women compared to obese men, lean men and lean women respectively (21.9±2.4 mg/g wet weight, 10.9±1.5, 9.8±2.1 and 10.9±2.4 mg/g, P<0.001). Among obese subjects of either gender IMTG did not increase along with reduced glycaemic control in terms of impaired fasting glucose and diabetes. Plasma insulin levels, which were similar among obese women with different glycaemic control levels, but much lower in lean women, paralleled the changes in IMTG among women. PBF was associated with IMTG in all subjects (P<0.001). In a linear model, sex (P<0.05) and PBF (P<0.05) independently explained variation in IMTG. Plasma free fatty acids (FFA) correlated with IMTG in all subjects (P<0.005).


Obese women display twice as much IMTG as obese men matched for BMI. Increased IMTG could be a pathophysiological element or a mere physiological phenomenon in feminine obesity ensuing prior to impaired glycaemic control, but associated with increased body fat, circulating FFA and insulin.

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Steen B Haugaard, Ove Andersen, Flemming Dela, Jens Juul Holst, Heidi Storgaard, Mogens Fenger, Johan Iversen and Sten Madsbad

Objectives: Lipodystrophy and insulin resistance are prevalent among human immunodeficiency virus (HIV)-infected patients on combined antiretroviral therapy (HAART). Aiming to provide a detailed description of the metabolic adverse effects of HIV-lipodystrophy, we investigated several aspects of glucose metabolism, lipid metabolism and β-cell function in lipodystrophic HIV-infected patients.

Methods: [3-3H]glucose was applied during euglycaemic hyperinsulinaemic clamps in association with indirect calorimetry in 43 normoglycaemic HIV-infected patients (18 lipodystrophic patients on HAART (LIPO), 18 patients without lipodystrophy on HAART (NONLIPO) and seven patients who were naïve to antiretroviral therapy (NAÏVE) respectively). β-cell function was evaluated by an intravenous glucose tolerance test.

Results: Compared with NONLIPO and NAÏVE separately, LIPO displayed markedly reduced ratio of limb to trunk fat (RLF; >34%, P < 0.001), hepatic insulin sensitivity (>40%, P < 0.03), incremental glucose disposal (>50%, P < 0.001) and incremental exogenous glucose storage (>50%, P < 0.05). Furthermore, LIPO displayed reduced incremental glucose oxidation (P < 0.01), increased clamp free fatty acids (P < 0.05) and attenuated insulin-mediated suppression of lipid oxidation (P < 0.05) compared with NONLIPO. In combined study groups, RLF correlated with hepatic insulin sensitivity (r = 0.69), incremental glucose disposal (r = 0.71) and incremental exogenous glucose storage (r = 0.40), all P < 0.01. Disposition index (i.e. first-phase insulin response to intravenous glucose multiplied by incremental glucose disposal) was reduced by 46% (P = 0.05) in LIPO compared with the combined groups of NONLIPO and NAÏVE, indicating an impaired adaptation of β-cell function to insulin resistance in LIPO.

Conclusion: Our data suggest that normoglycaemic lipodystrophic HIV-infected patients display impaired glucose and lipid metabolism in multiple pathways involving liver, muscle tissue and β-cell function.