Recently, some studies have focused on the relationship between dietary protein intake and the risk of type 2 diabetes mellitus (T2DM), but the conclusions have been inconsistent. Therefore, in this paper, a systematic review and meta-analysis of cohort studies regarding protein consumption and T2DM risk are conducted in order to present the association between them. We searched the PubMed and Embase databases for cohort studies on dietary protein, high-protein food consumption and risk of T2DM, up to July 2017. A summary of relative risks was compiled by the fixed-effect model or random-effect model. Eleven cohort studies regarded protein intake and T2DM (52,637 cases among 483,174 participants). The summary RR and 95% CI (Confidence Interval) of T2DM was 1.12 (1.08–1.17) in all subjects, 1.13 (1.04–1.24) in men, and 1.09 (1.04–1.15) in women for total protein;1.14 (1.09–1.19) in all subjects, 1.23 (1.09–1.38) in men, and 1.11 (1.03–1.19) in women for animal protein; 0.96 (0.88–1.06) in all subjects, 0.98 (0.72–1.34) in men, and 0.92 (0.86–0.98) in women for plant protein. We also compared the association between different food sources of protein and the risk of T2DM. The summary RR (Relative Risk) and 95% CI of T2DM was 1.22 (1.09–1.36) for red meat, 1.39 (1.29–1.49) for processed meat, 1.03 (0.89–1.17) for fish, 1.03 (0.64–1.67) for egg, 0.89 (0.84–0.94) for total dairy products, 0.87 (0.78–0.96) for whole milk, 0.83 (0.70–0.98) for yogurt, 0.74 (0.59–0.93) in women for soy. This meta-analysis shows that total protein and animal protein could increase the risk of T2DM in both males and females, and plant protein decreases the risk of T2DM in females. The association between high-protein food types and T2DM are also different. Red meat and processed meat are risk factors of T2DM, and soy, dairy and dairy products are the protective factors of T2DM. Egg and fish intake are not associated with a decreased risk of T2DM. This research indicates the type of dietary protein and food sources of protein that should be considered for the prevention of diabetes.

Although hyperuricemia and insulin resistance significantly correlated, their temporal sequence and how the sequence influence on future risk of hypertension are largely unknown. This study assessed temporal relationship between uric acid and insulin resistance and its impact on future risk of hypertension by examining a longitudinal cohort including 8543 subjects aged 20 to 74 years from China, with an average follow-up of 5.3 years. Measurements of fasting uric acid, as well as fasting and 2-hour serum glucose and insulin, were obtained at baseline and follow-up. Indicators of hepatic and peripheral insulin resistance were calculated. Cross-lagged panel and mediation analysis were used to examine the temporal relationship between uric acid and insulin resistance and its impact on follow-up hypertension. After adjusting for covariates, the cross-lagged path coefficients ( β ₁ values) from baseline uric acid to follow-up insulin resistance indices were significantly greater than path coefficients ( β ₂ values) from baseline insulin resistance indices to follow-up uric acid ( β ₁ =0.110 versus β ₂ =0.017; P <0.001, for hepatic insulin resistance; β ₁ =−0.208 versus β ₂ =−0.021; P <0.001, for peripheral insulin resistance). The path coefficients from baseline uric acid to follow-up insulin resistance indices in the hypertensive group were significantly greater than that in the normotensive group ( P <0.001 for the difference of β ₁ values in the 2 groups). Insulin resistance partially mediated the effect of uric acid on subsequent hypertension, and the mediation effect of peripheral insulin resistance was significantly greater than that of hepatic insulin resistance (31.3% versus 13.2%; P <0.001, for the difference of mediation effects). These findings provide evidence that higher uric acid levels probably precede insulin resistance, and peripheral insulin resistance likely plays a more important role in the development of hypertension than hepatic insulin resistance does.

Induction of adipocyte apoptosis has been postulated as a novel strategy with which to treat obesity. The effects of curcumin, a polyphenol compound, on the apoptotic signaling pathway in SW872 adipocytes were investigated in the present study. The results showed that cell viability decreased following curcumin treatment in a time- and dose-dependent manner. The results from a single-stranded DNA ELISA assay indicated that curcumin causes the number of apoptotic cells to increase in a concentration-dependent manner. In addition, curcumin treatment resulted in an increased expression of Bax, and a decrease in that of of Bcl-2, with a concomitant upregulation of the Bax/Bcl-2 ratio. Curcumin treatment also led to the release of cytochrome c from mitochondria into the cytosol. Similarly, caspase-dependent poly (ADP) ribose polymerase (PARP) cleavage by curcumin was observed in the current study. In conclusion the results indicate that curcumin is an effective therapeutic agent with which to induce apoptosis in adipocytes. This effect is, in part, mediated through the mitochondrial pathway, which involves upregulation of the Bax/Bcl-2 ratio, cytochrome c release, activation of caspase-3 and the cleavage of PARP.

Results of longitudinal researches regarding the temporal relationship between dyslipidemia and insulin resistance (IR) are inconsistent. This study assessed temporal relationships of blood lipids with IR and determined whether there are any mediating effects existed in these temporal relationships. This study examined a longitudinal cohort of 3325 subjects aged 20–74 years from China with an average of 4.2 years follow-up. Measurements of fasting blood lipids, as well as fasting and 2-h serum glucose and insulin, were obtained at two time points. The Gutt index and HOMA-IR were calculated as indicators of peripheral IR and hepatic IR. A cross-lagged path analysis was performed to examine the temporal relationships between blood lipids and IR. A mediation analysis was used to examine mediating effect. After adjusting for covariates, the cross-lagged path coefficients from baseline TG and HDL-C to follow-up Gutt index were significantly greater than those from baseline Gutt index to follow-up TG and HDL-C (β1 = −0.131 vs β2 = −0.047, P < 0.001 for TG; β1 = 0.134 vs β2 = 0.023, P < 0.001 for HDL-C). The path coefficients from baseline TG and HDL-C to follow-up 2-h insulin were significantly greater than those from baseline 2-h insulin to follow-up TG and HDL-C (β1 = 0.125 vs β2 = 0.040, P < 0.001 for TG; β1 = −0.112 vs β2 = −0.026, P < 0.001 for HDL-C). 2-h insulin partially mediated the effect of TG/HDL-C on Gutt index with a 59.3% mediating effect for TG and 61.0% for HDL-C. These findings provide strong evidence that dyslipidemia probably precede peripheral IR and that 2-h insulin partially mediates this unidirectional temporal relationship.