Association of vitamin D and cognition in people with type 2 diabetes: a systematic review.

CONTEXT: There is a high prevalence of vitamin D deficiency and impaired cognitive function in people with type 2 diabetes mellitus (T2DM). OBJECTIVE: To critically and systematically review the literature on the association between vitamin D status and cognitive performance in people with type 2 diabetes. DATA SOURCES: This review was conducted according to PRISMA recommendations. MEDLINE, SCOPUS, the Cochrane Library, and Web of Science databases were searched using the terms "Diabetes Mellitus, Type 2", "Cognitive Function", and "Vitamin D". DATA EXTRACTION: Eight observational and 1 randomized study were included, containing data of 14 648 adult and elderly individuals (19-74 y). All extracted data were compiled, compared, and critically analyzed. DATA ANALYSIS: There is no strong evidence that lower serum concentrations of vitamin D and vitamin D-binding protein are associated with worsening cognitive function in individuals with T2DM. Vitamin D supplementation (12 wk) improved the scores of some executive functioning tests, although there was no difference between low doses (5000 IU/wk) and high doses (50 000 IU/wk). CONCLUSIONS: There is no high-quality evidence demonstrating an association between vitamin D status and cognitive function, or clinical benefits on cognition from vitamin D supplementation in individuals with T2DM. Future studies are needed. Systematic Review Registration: PROSPERO registration no. CRD42021261520.

Genetic deletion of Mas receptor in FVB/N mice impairs cardiac use of glucose and lipids.

Angiotensin-(1-7) is a biologically active product of the renin-angiotensin system cascade and exerts inhibitory effects on inflammation, vascular and cellular growth mechanisms signaling through the G protein-coupled Mas receptor. The major purpose of the present study was to investigate the use of glucose and fatty acids by cardiac tissue in Mas knockout mice models. Serum levels of glucose, lipids, and insulin were measured in Mas-deficient and wild-type FVB/N mice. To investigate the cardiac use of lipids, the lipoprotein lipase, the gene expression of peroxisome proliferator-activated receptor alpha; carnitine palmitoyltransferase I and acyl-CoA oxidase were evaluated. To investigate the cardiac use of glucose, the insulin signaling through Akt/GLUT4 pathway, glucose-6-phosphate (G-6-P) and fructose-6-phosphate (F-6-P) glycolytic intermediates, in addition to ATP, lactate and the glycogen content were measured. Despite normal body weight, cholesterol and insulin, Mas-Knockout mice presented hyperglycemia and hypertriglyceridemia, impaired insulin signaling, through reduced phosphorylation of AKT and decreased translocation of GLUT4 in response to insulin, with subsequent decrease of the cardiac G-6-P and F-6-P. Lactate production and glycogen content were not altered in Mas-KO hearts. Mas-KO presented reduced cardiac lipoprotein lipase activity and decreased translocation of CD36 in response to insulin. The expression of peroxisome proliferator-activated receptor alpha and carnitine palmitoyltransferase I genes were lower in Mas-KO animals compared to wild-type animals. The ATP content of Mas-KO hearts was smaller than in wild-type. The present results suggest that genetic deletion of Mas produced a devastating effect on cardiac use of glucose and lipids, leading to lower energy efficiency in the heart.