Background: Currently the treatment of non-alcoholic fatty liver disease (NAFLD) is based on weight loss through lifestyle changes, such as exercise combined with calorie-restricted dieting. Objectives: To assess the effects of a commercially available weight loss program based on a very low-calorie ketogenic diet (VLCKD) on visceral adipose tissue (VAT) and liver fat content compared to a standard low-calorie (LC) diet. As a secondary aim, we evaluated the effect on liver stiffness measurements. Methods: Open, randomized controlled, prospective pilot study. Patients were randomized and treated either with an LC or a VLCKD and received orientation and encouragement to physical activity equally for both groups. VAT, liver fat fraction, and liver stiffness were measured at baseline and after 2 months of treatment using magnetic resonance imaging. Paired t-tests were used for comparison of continuous variables between visits and unpaired test between groups. Categorical variables were compared using the χ 2-test. Pearson correlation was used to assess the association between VAT, anthropometric measures, and hepatic fat fraction. A significance level of the results was established at p < 0.05. Results: Thirty-nine patients (20 with VLCKD and 19 with LC) were evaluated at baseline and 2 months of intervention. Relative weight loss at 2 months was −9.59 ± 2.87% in the VLCKD group and −1.87 ± 2.4% in the LC group (p < 0.001). Mean reductions in VAT were −32.0 cm 2 for VLCKD group and −12.58 cm 2 for LC group (p < 0.05). Reductions in liver fat fraction were significantly more pronounced in the VLCKD group than in the LC group (4.77 vs. 0.79%; p < 0.005). Cunha et al. VLCKD for Visceral Fat and NAFLD Conclusion: Patients undergoing a VLCKD achieved superior weight loss, with significant VAT and liver fat fraction reductions when compared to the standard LC diet. The weight loss and rapid mobilization of liver fat demonstrated with VLCKD could serve as an effective alternative for the treatment of NAFLD.

Based on the current ISCD criteria, bone density evaluation in women with prolactinoma reveals bone loss, especially of trabecular type. Bone density in these patients was particularly associated with the duration of amenorrhea, which reinforces the importance of the adequate disease control in women with prolactinoma in order to avoid complications of this disease.

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Objective: This study aimed to evaluate the occurrence and clinical predictors of subclinical atherosclerosis in asymptomatic, young adult women with type 1 DM. Subjects and methods: The study included 45 women with type 1 diabetes mellitus (DM) (aged 36 ± 9 years) who underwent carotid Doppler ultrasound evaluation to determine the carotid artery intima-media thickness (CIMT) and to assess the occurrence of carotid artery plaques. Insulin sensitivity was assessed by estimated glucose disposal rate (eGDR), and metabolic syndrome (MS) was defined by the World Health Organization criteria. Results: The cohort had a mean age of 36 ± 9 years, diabetes duration of 18.1 ± 9.5 years, and body mass index (BMI) of 24.6 ± 2.4 kg/m 2 . MS was present in 44.4% of the participants. The CIMT was 0.25 ± 0.28 mm, and the prevalence of carotid artery plaques was 13%. CIMT correlated positively with hypertension (p = 0.04) and waist-to-hip ratio (r = 0.37, p = 0.012). The presence of carotid artery plaques correlated positively with age (p = 0.018) and hypertension (p = 0.017). eGDR correlated negatively with CIMT (r = -0.39, p = 0.009) and carotid plaques (p = 0.04). Albuminuria showed a correlation trend with CIMT (p = 0.06). Patients with carotid artery plaques were older, had a higher prevalence of hypertension, and lower eGDR. No correlation was found between CIMT and carotid plaques with diabetes duration, MS, BMI, cholesterol profile, glycated hemoglobin, high-sensitivity C-reactive protein, or fibrinogen. Conclusion: Insulin resistance, central obesity, hypertension, and older age were predictors of subclinical atherosclerosis in asymptomatic, young adult women with type 1 DM. Arch Endocrinol Metab. 2017;61(2):115-21.