Efficacy of an Educational Intervention for Sodium Restriction in Patients with Hypertension: A Randomized Controlled Trial.

There is sound evidence showing the efficacy of non-pharmacological interventions in lowering blood pressure (BP); however, adherence is usually poor. Interventions to induce behavioral changes aim to improve the ability to read labels, choose foods, and eat low-sodium meals, reinforcing adherence to sodium restriction. In this randomized parallel-controlled trial, we assessed the effectiveness of an educational intervention using the Dietary Sodium Restriction Questionnaire (DSRQ) scores. A follow-up period of 6 months was conducted. Participants were randomized into (1) an educational intervention provided by a registered dietitian on individual visits and dietary planning; (2) a control group with the usual care and dietary recommendations. Patients underwent 24-h ambulatory BP monitoring, 12-h fasting blood tests, spot urine collection, and assessment using DSRQ. We randomized 120 participants (67.5% women and 68.3% Caucasians), and 25 participants were lost to follow-up. The 24-h sodium urinary excretion changed in the control (Δ -1610 mg/day; 95% confidence interval [CI] -1800 to -1410) and intervention groups (Δ -1670 mg/day; 95% CI -1800 to -1450) over time. There was no significant difference in the 24-h estimated sodium between groups. In hypertensive patients, DSRQ-based educational intervention is effective for improving the ability to detect and overcome obstacles to a low-sodium restriction diet but is as effective as dietary recommendations for lowering sodium.

Effects of transcranial direct current stimulation associated with hypocaloric diet on glucose homeostasis in obesity.

OBJECTIVE: The aim of this study was to test the effects of repetitive active transcranial direct current stimulation (tDCS) over the right dorsolateral prefrontal cortex (rDLPFC) associated with a hypocaloric diet on glucose homeostasis in people with excessive weight. METHODS: Adults with overweight or obesity were selected in a randomized, double-blind pilot study to complete 4 weeks (20 sessions) of fixed-dose tDCS (2 mA, 20 minutes) delivered over the rDLPFC and associated with a standard hypocaloric diet. Participants were randomly assigned (1:1) and stratified by sex to the active tDCS group (active) or the sham tDCS group (sham). Changes in glucose homeostasis were assessed in a 4-hour liquid meal tolerance test, performed before and after the intervention. RESULTS: Twenty-eight participants were randomized (79% with obesity; mean [SD] age 37.6 [5.8] years). After the intervention, fasting plasma glucose (mean [95% CI], -7.8 mg/dL [-14.0 to -1.6]) and insulin levels (-7.7 µIU/mL [-13.9 to -1.6]) decreased in the active compared with the sham. Similarly, the Matsuda insulin sensitivity index increase in the active (4.7 pmol-1  × mmol-1 [1.6 to 7.8]) compared with the sham (0.6 pmol-1  × mmol-1 [-1.4 to 3.2]). CONCLUSIONS: Repetitive, active tDCS over the rDLPFC could be a promising noninvasive technique to improve glucose homeostasis in individuals with overweight or obesity on a low-calorie diet, highlighting the importance of investigating this intervention modality in individuals with type 2 diabetes mellitus.

Kinin B1 receptor deficiency protects mice fed by cafeteria diet from abnormal glucose homeostasis.

The kallikrein-kinin system has been implicated in body weight and glucose homeostasis. Their major effectors act by binding to the kinin B2 and B1 receptors. It was assessed the role of the kinin B1 receptor in weight and glucose homeostasis in B1 receptor knockout mice (B1RKO) subjected to a cafeteria diet (CAF). Wild-type (WT) and B1RKO male mice (C57BL/6 background; 8 weeks old) were fed a standard diet (SD) or CAF for 14 weeks, ad libitum, and four groups were formed: WT-SD; B1RKO-SD; WT-CAF; B1RKO-CAF. Body weight and food intake were assessed weekly. It was performed glucose tolerance (GTT) and insulin tolerance tests (ITT), and HOMA-IR, HOMA-ß and HOMA-ß* 1/HOMA-IR were calculated. Islets from WT and B1RKO were isolated in order to measure the insulin secretion. Western blot was used to assess the hepatic AKT phosphorylation and qPCR to assess gene expression. CAF induced a higher body mass gain in B1RKO compared to WT mice. CAF diet increased epididymal fat depot mass, hepatic fat infiltration and hepatic AKT phosphorylation in both genotypes. However, B1RKO mice presented lower glycemic response during GTT when fed with CAF, and a lower glucose decrease in the ITT. This higher resistance was overcomed with higher insulin secretion when stimulated by high glucose, resulting in higher glucose uptake in the GTT when submitted to CAF, despite lower insulin sensitivity. Islets from B1RKO delivered 4 times more insulin in 3-month-old mice than islets from WT. The higher insulin disposition index and high insulin delivery of B1RKO can explain the decreased glucose excursion during GTT. In conclusion, CAF increased the ß-cell function in B1RKO mice, compensated by the diet-induced insulin resistance and resulting in a healthier glycemic response despite the higher weight gain.