Objectives Obesity and insulin resistance (IR) are interrelated in a range of ways. The IR-obesity relationship is not a cause-and-effect association. Molecular biology research has made tremendous strides in discovering contributors to find this association. Genes that control adipocyte function such as caveolin-1 (CAV1); probably interact in the pathogenesis of human IR in this context. The involvement of CAV1 in glucose/lipid homeostasis is revealed and could modify the signaling of the insulin receptor. We examined the association between CAV1 and insulin signaling in modifying dyslipidemia and fat composition in overweight and obese women with a prevalent variant in the CAV1 gene. Results Minor allele carriers were slightly older and had higher BMI (p = 0.02), FMI (p = 0.006), and VLF (p = 0.01) values; and tended to have lower total cholesterol TC (p = 0.04), low-density lipoprotein cholesterol (LDL-C) (p = 0.001) and high-density lipoprotein cholesterol (HDL-C) (p = 0.003). HOMA-IR levels predicted fat mass index (FMI) 0.47 (0.08, 0.87), visceral fat level (VFL) 0.65 (0.23, 1.07), TC 6.82 (1.76, 11.88) and HDL-C − 1.663 (− 3.11, − 0.214) only between minor allele carriers in adjusted models. (β, CI). Our results cast a new light on the IR mechanism and future studies will elucidate the clinical relevance of CAV1-IR in patients with dyslipidemia and high fat composition.

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Background Metabolic syndrome (MetS) is associated with an increased risk of morbidity and mortality in almost all chronic diseases. The most frequent methods for the calculation of a continuous MetS (cMetS) score have used the standardized residuals in linear regression (z-score). Recently, emerging data suggest that one of the main genetic targets is the CAV1, which plays a crucial role in regulating body fat distribution. This study is designed to investigate the relationship between CAV1 rs3807992 genotypes and cMetS, and to determine whether body fat distribution plays a mediating role in this regard. Methods The current cross-sectional study was conducted on 386 overweight and obese females. The CAV1 rs3807992 and body composition were measured by the PCR–RFLP method and bioelectrical impedance analysis, respectively. Serum profile of HDL-C, TGs, FPG, and Insulin were measured by standard protocols. Results GG allele carriers had significantly lowered Z-MAP (p = 0.02), total cMetS (p = 0.03) and higher Z-HDL (p = 0.001) compared with (A) allele carriers. There was a significant specific indirect effect (standardized coefficient = 0.19; 95% CI 0.01–0.4) of Visceral fat level (VFL). Although, total body fat was significantly associated with CAV1 rs3807992 and cMetS, the specific indirect effect was not significant (standardized coefficient = 0.21; 95% CI − 0.006, 0.44). VFL contributed to significant indirect effects of 35% on the relationship between CAV1 and cMetS. Conclusion Higher visceral adipose tissue may affect the relationship between CAV1 and cMetS. Although CAV1 rs3807992 is linked to VFL in our study, the influence of this polymorphism on MetS is not via total fat.

Background: Interleukin 6 is an important biomarker for distinguishing high-risk and low-risk patients, and is a constituent of the Nutrition Risk in the Critically III (NUTRIC) Score. Studies have indicated the beneficial effects of vitamin C on lowering IL-6 levels and reducing cytokine storm. However, there is still controversy about the exact effect, appropriate route, and dose of vitamin C usage. This meta-analysis was conducted to evaluate the current evidence base relating to vitamin C intervention on decreasing IL-6 levels. Methods: A systematic search was performed in PubMed, Scopus, Google Scholar, and Cochran databases, from database inception to July 3 rd 2021, to obtain any possible randomized clinical trial for inclusion. After screening and removing unrelated and duplicate articles, 24 eligible articles remained for statistical analysis. Results: We found a significant lowering effect of vitamin C supplementation on IL-6 levels via peroral (PO) (WMD ¼ -0.29 pg/l,

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