Effectiveness of metformin for the reversal of cold-ischemia-induced damage in hepatosteatosis.

BACKGROUND: Primary dysfunction and rejection are more common in donor liver tissues with steatosis. AMP-activated protein kinase (AMPK) assumes organ-protective functions during ischemia. Metformin was used for the activation of AMPK in hepatocytes. The aim of this study is to investigate the effectiveness of metformin administration for the reversal of cold-ischemia-induced damage in hepatosteatosis. MATERIAL AND METHODS: Seven-week-old C7BL56 male-mice (n = 109) were separated into four groups depending on diet type and metformin use. A specific diet model was followed for 10 weeks to induce hepatosteatosis. A group of the animals was administered with metformin for the last four weeks via oral gavage. After resection, the liver tissues were perfused and kept for 0-6-12-24 h in the UW solution. Histopathological examinations were performed, and Western blot was utilized to analyze p-AMPK and AMPK expression levels. RESULTS: Hepatosteatosis decreased significantly with metformin. The steatotic liver group had more prominent pericentral inflammation, necrosis as well as showing a decreased and more delayed AMPK response than the non-fat group. All these alterations could be corrected using metformin. CONCLUSION: Metformin can increase the resistance of livers with hepatosteatosis to cold-ischemia-induced damage, which in turn may pave the way for successful transplantation of fatty living-donor livers.

A New Approach to Polycystic Ovary Syndrome and Related Cardio-metabolic Risk Factors: Dietary Polyphenols.

PURPOSE OF REVIEW: Polycystic ovarian syndrome (PCOS) is a common endocrine disease characterized by ovulatory dysfunction, hyperandrogenism, and polycystic ovarian morphology and causing various reproductive, metabolic, cardiovascular, oncological, and psychological complications. Recent meta-analyses and systemic reviews showed that PCOS increases the risk factor for various cardio-metabolic complications like insulin resistance, type II diabetes mellitus, dyslipidemia, metabolic syndrome, hypertension, and endothelial dysfunction. In addition to these, it was suggested that chronic low-grade inflammation and oxidative stress are the underlying mechanisms of PCOS-mediated metabolic consequences and might trigger cardio-metabolic risk in women with PCOS. At this point, there is substantial evidence to suggest that various non-nutrient food components modulate cardio-metabolic health together with inflammation and oxidative stress. RECENT FINDINGS: Increasing the intake of dietary polyphenols might reduce oxidative stress and inflammation and thus alleviate the risk of metabolic, endothelial, and cardiovascular disorders. Nowadays, there are an increasing number of studies related to the effects of dietary polyphenols on PCOS and its accompanying cardio-metabolic disturbances. Currently, there is a cumulative number of studies connected to the effects of dietary polyphenols on PCOS and accompanying cardio-metabolic disturbances. However, there is a lack of knowledge in combining the probable mechanisms of dietary polyphenols on PCOS and related cardio-metabolic consequences. Thus, the effects of dietary polyphenols on PCOS and accompanying cardio-metabolic disturbances need to be discussed and evaluated with underlying mechanisms. Consequently, this review was written to reveal the potential effects of dietary polyphenols on PCOS and related metabolic and cardiovascular risk factors in all their aspects.