Intramyocellular lipid (IMCL) storage is considered a local marker of whole body insulin resistance; because increments of body weight are supposed to impair insulin sensitivity, this study was designed to assess IMCL content, lipid oxidation, and insulin action in individuals with a moderate increment of body fat mass and no family history of diabetes. We studied 14 young, nonobese women with body fat <30% (n = 7) or >30% (n = 7) and 14 young, nonobese men with body fat <25% (n = 7) or >25% (n = 7) by means of the euglycemic-insulin clamp to assess whole body glucose metabolism, with indirect calorimetry to assess lipid oxidation, by localized (1)H NMR spectroscopy of the calf muscles to assess IMCL content, and with dual-energy X-ray absorptiometry to assess body composition. Subjects with higher body fat had normal insulin-stimulated glucose disposal (P = 0.80), IMCL content in both soleus (P = 0.22) and tibialis anterior (P = 0.75) muscles, and plasma free fatty acid levels (P = 0.075) compared with leaner subjects in association with increased lipid oxidation (P < 0.05), resting energy expenditure (P = 0.046), resting oxygen consumption (P = 0.049), and plasma leptin levels (P < 0.01) in the postabsorptive condition. In conclusion, in overweight subjects, preservation of insulin sensitivity was combined with increased lipid oxidation and maintenance of normal IMCL content, suggesting that abnormalities of these factors may mutually determine the development of insulin resistance associated with weight gain.

In conclusion, TELEDIABE proposes a new system for the management of patients with type 1 diabetes mellitus.

, on protease inhibitors and nucleoside analog RT inhibitors) and 12 healthy subjects were studied. HIV-1 patients had a total body fat content (assessed by dual-energy X-ray absorptiometry) similar to that of controls (22 Ϯ 1 vs. 23 Ϯ 2%; P ϭ 0.56), with a topographic fat redistribution characterized by reduced fat content in the legs (18 Ϯ 2 vs. 32 Ϯ 3%; P Ͻ 0.01) and increased fat content in the trunk (25 Ϯ 2 vs. 19 Ϯ 2%; P ϭ 0.03). In HIV-positive patients, insulin sensitivity (assessed by QUICKI) was markedly impaired (0.341 Ϯ 0.011 vs. 0.376 Ϯ 0.007; P ϭ 0.012). HIV-positive patients also had increased total plasma cholesterol (216 Ϯ 20 vs. 174 Ϯ 9 mg/dl; P ϭ 0.05) and triglyceride (298 Ϯ 96 vs. 87 Ϯ 11 mg/dl; P ϭ 0.03) concentrations. Muscular triglyceride content assessed by means of 1 H NMR spectroscopy was higher in HIV patients in soleus [92 Ϯ 12 vs. 42 Ϯ 5 arbitrary units (AU); P Ͻ 0.01] and tibialis anterior (26 Ϯ 6 vs. 11 Ϯ 3 AU; P ϭ 0.04) muscles; in a stepwise regression analysis, it was strongly associated with QUICKI (R 2 ϭ 0.27; P Ͻ 0.0093). Even if the basal metabolic rate (assessed by indirect calorimetry) was comparable to that of normal subjects, postabsorptive lipid oxidation was significantly impaired (0.30 Ϯ 0.07 vs. 0.88 Ϯ 0.09 mg⅐kg Ϫ1 ⅐min Ϫ1

Ultrasound scan can help identify and characterize the lipohypertrophic areas and this might be useful to improve glycemic control.

Diabetes mellitus was diagnosed in 16 out of 1011 HIV-positive patients over a median follow-up of 289 days (person-year incidence 2.06, 95% confidence interval 1.18-3.33). Significant risk factors for the onset of diabetes were older age and antiretroviral therapy with stavudine or indinavir. Older men with HIV infection should be considered at higher risk of diabetes, and caution maybe warranted in the use of both indinavir and stavudine in these patients.