Patients with metabolic syndrome are at an increased risk of developing type 2 diabetes and cardiovascular diseases. The principal risk factor for development of metabolic syndrome is obesity, defined as a state of pathological hyperplasia or/and hypertrophy of adipose tissue. The number of mature adipocytes is determined by adipocyte differentiation from preadipocytes. The purpose of the present study is to investigate the effects of curcumin on adipogenesis and the underlying mechanism. To examine cell toxicity of curcumin, 3T3-L1 preadipocytes were treated with 0–50 µM curcumin for 24, 48, or 72 h, then cell viability was measured using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. The effect of curcumin on the cell cycle was determined by flow cytometry. Curcumin-induced cell apoptosis was determined by the TUNEL assay and curcumin-induced caspase activation was measured by immunoblotting. The effect of curcumin on adipocyte differentiation was determined by measuring mitotic clonal expansion (MCE), expression of adipogenic transcription factors, and lipid accumulation. Results showed the viability of preadipocytes was significantly decreased by treatment with 30 µM curcumin, a concentration that caused apoptosis in preadipocytes, as assessed by the TUNEL assay, and caused activation of caspases 8, 9, and 3. A non-cytotoxic dose of curcumin (15 µM) inhibited MCE, downregulated the expression of PPARγ and C/EBPα, prevented differentiation medium-induced β-catenin downregulation, and decreased the lipid accumulation in 3T3-L1 adipocytes. In conclusion, our data show that curcumin can induce preadipocyte apoptosis and inhibit adipocyte differentiation, leading to suppression of adipogenesis.

Background: Hamstring weakness has been associated with an increased risk of hamstring strain, a common sports injury that occurs when athletes perform actions such as quick sprints. The hamstring complex comprises three distinct muscles: the long and short heads of the bicep femoris, the semimembranosus, and the semitendinosus. Methods: The researchers collected the data from different electronic databases: PubMed, Google Scholar, and the Web of Science. Results: Many studies have been conducted on the numerous benefits of hamstring strength, in terms of athletic performance and injury prevention. Isotonic and isometric exercises are commonly used to improve hamstring strength, with each exercise type having a unique effect on the hamstring muscles. Isotonic exercise improves the muscles’ strength, increasing their ability to resist any force, while isometric training increases strength and the muscles’ ability to produce power by changing the muscle length. Conclusions: These exercises, when performed at low intensity, but with high repetition, can be used by the healthy general population to prepare for training and daily exercise. This can improve hamstring muscle strength and flexibility, leading to enhanced performance and reduced injury risk.

Polycystic ovary syndrome (PCOS), which affects 5–10% of women of reproductive age, is associated with reproductive and metabolic disorders, such as chronic anovulation, infertility, insulin resistance, and type 2 diabetes. However, the mechanism of PCOS is still unknown. Therefore, this study used a letrozole-exposed mouse model in which mice were orally fed letrozole for 20 weeks to investigate the effects of letrozole on the severity of reproductive and metabolic consequences and the expression of cysteine–cysteine motif chemokine receptor 5 (CCR5) in letrozole-induced PCOS mice. The letrozole-treated mice showed a disrupted estrous cycle and were arrested in the diestrus phase. Letrozole treatment also increased plasma testosterone levels, decreased estradiol levels, and caused multicystic follicle formation. Furthermore, histological analysis of the perigonadal white adipose tissue (pgWAT) showed no significant difference in the size and number of adipocytes between the letrozole-treated mice and the control group. Further, the letrozole-treated mice demonstrated glucose intolerance and insulin resistance during oral glucose and insulin tolerance testing. Additionally, the expression of CCR5 and cysteine-cysteine motif ligand 5 (CCL5) were significantly higher in the pgWAT of the letrozole-treated mice compared with the control group. CCR5 and CCL5 were also significantly correlated with the homeostasis model assessment of insulin resistance (HOMA-IR). Finally, the mechanisms of insulin resistance in PCOS may be caused by an increase in serine phosphorylation and a decrease in Akt phosphorylation.

Plasma and tissue zinc ion levels are associated with the development of obesity. Previous studies have suggested that zinc ions may regulate adipocyte metabolism and that nitric oxide (NO) plays a pivotal role in the regulation of adipocyte physiology. Our previous study showed that chronic NO deficiency causes a significant decrease in adipose tissue mass in rats. Studies also suggested that zinc ions play an important modulatory role in regulating NO function. This study aims to explore the role of zinc ions in NO-regulated adipocyte differentiation. We hypothesized that NO could increase intracellular Zn²⁺ level and then stimulate adipocyte differentiation. ZnCl₂ and the NO donor, NONOate, were used to explore the effects of Zn²⁺ and NO on adipocyte differentiation. Regulatory mechanisms of NO on intracellular Zn²⁺ mobilization were determined by detection. Then, Zn²⁺-selective chelator TPEN was used to clarify the role of intracellular Zn²⁺ on NO-regulated adipocyte differentiation. Furthermore, the relationship between adipocyte size, Zn²⁺ level, and NOS expression in human subcutaneous fat tissue was elucidated. Results showed that both ZnCl₂ and NO stimulated adipocyte differentiation in a dose-dependent manner. NO stimulated intracellular Zn²⁺ mobilization in adipocytes through the guanylate cyclase (GC)/cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) pathway, and NO-stimulated adipocyte differentiation was Zn²⁺-dependent. In human subcutaneous adipose tissue, adipocyte size was negatively correlated with expression of eNOS. In conclusion, NO treatment stimulates intracellular Zn²⁺ mobilization through the GC/cGMP/PKG pathway, subsequently stimulating adipocyte differentiation.