Observational studies classically find an inverse relationship between human plasma 25-hydroxyvitamin D concentration and obesity. However, interventional and genetic studies have failed to provide clear conclusions on the causal effect of vitamin D on obesity/adiposity. Likewise, vitamin D supplementation in obese rodents has mostly failed to improve obesity parameters, whereas several lines of evidence in rodents and prospective studies in humans point to a preventive effect of vitamin D supplementation on the onset of obesity. Recent studies investigating the impact of maternal vitamin D deficiency in women and in rodent models on adipose tissue biology programming in offspring further support a preventive metabolically driven effect of vitamin D sufficiency. The aim of this review is to summarize the state of the knowledge on the relationship between vitamin D and obesity/adiposity in humans and in rodents and the impact of maternal vitamin D deficiency on the metabolic trajectory of the offspring.

The central control of energy balance involves a strongly regulated neuronal network within the hypothalamus and the brainstem. In these structures, pro-opiomelanocortin (POMC) neurons are known to decrease food intake and to increase energy expenditure. Thus, leptin, a peripheral signal that relays information regarding body fat content, modulates the activity of POMC neurons. MicroRNAs (miRNAs) are short non-coding RNAs of 22–26 nucleotides that post-transcriptionally interfere with target gene expression by binding to their mRNAs. It has been demonstrated that leptin is able to modulate the expression of miRNAs (miR-383, miR-384-3p, and miR-488) that potentially target POMC mRNA. However, no study has identified the transduction pathways involved in this effect of leptin on miRNA expression. In addition, miRNAs targeting POMC mRNAs are not clearly identified. In this work, using in vitro models, we have identified and confirmed that miR-383, miR-384-3p, and miR-488 physically binds to the 3′ untranslated (3′UTR) regions of POMC mRNA. Importantly, we show that leptin inhibits these miRNAs expression by different transduction pathways. Taken together, these results allowed us to highlight the miRNA involvement in the regulation of POMC expression downstream of the leptin signaling and satiety signal integration.

Hepatic steatosis may be caused by type 2 diabetes or obesity and is one of the origins of chronic liver disease. A non-invasive technique based on microwave propagation can be a good solution to monitor hepatic tissue pathologies. The present work is devoted to the dielectric permittivity measurements in healthy and fatty liver in the microwave range. A mouse model following normal and high sugar/glucose (HFS) diets was used. We demonstrated the change in the triglyceride and glucose concentration in the hepatic tissue of HFS diet mice. The difference in the dielectric permittivity of healthy and fatty liver was observed in the range from 100 MHz to 2 GHz. The dielectric permittivity was found to be 42 in the healthy tissue and 31 in the fatty liver tissue at 1 GHz. The obtained results demonstrate that dielectric permittivity can be a sensitive tool to distinguish between healthy and fatty hepatic tissue.