Abstract:Leptin and adiponectin, the main metabolic products of adipose tissue, have been implicated in a wide spectrum of human diseases. Given the frequent presence of hepatic steatosis in several chronic liver diseases, there is currently increasing interest in the role of these adipokines in the development of hepatic steatosis and also in necroinflammation and fibrosis, mostly in patients with nonalcoholic fatty liver disease or chronic hepatitis C. According to experimental data, reduced adiponectin levels and in… Show more
“…Existing studies suggest hypoadiponectinemia in NAFLD enhances insulin resistance by decreasing hepatic insulin sensitivity [41] and increasing production of the inflammatory protein, tumor necrosis factor-α [42]. Hypoadiponectinemia may perpetuate hepatic fat accumulation through an influx of free fatty acids into the liver resulting in hepatic steatosis [42,43]. Japanese women with NAFLD, defined by ultrasound, and mean ALT level of 45 U/L had significantly lower adiponectin concentration compared to those without NAFLD (7.2 vs. 9.0 ug/mL, p <0.005) [26].…”
BACKGROUND-Studies have shown alanine aminotransferase (ALT), a marker for nonalcoholic fatty liver disease (NAFLD), to predict type 2 diabetes (T2DM).
“…Existing studies suggest hypoadiponectinemia in NAFLD enhances insulin resistance by decreasing hepatic insulin sensitivity [41] and increasing production of the inflammatory protein, tumor necrosis factor-α [42]. Hypoadiponectinemia may perpetuate hepatic fat accumulation through an influx of free fatty acids into the liver resulting in hepatic steatosis [42,43]. Japanese women with NAFLD, defined by ultrasound, and mean ALT level of 45 U/L had significantly lower adiponectin concentration compared to those without NAFLD (7.2 vs. 9.0 ug/mL, p <0.005) [26].…”
BACKGROUND-Studies have shown alanine aminotransferase (ALT), a marker for nonalcoholic fatty liver disease (NAFLD), to predict type 2 diabetes (T2DM).
“…Patients with MetS and/or T2DM have low circulating adiponectin levels [86,87] . These are also decreased in patients with NAFLD, possibly due to enhanced hepatic insulin resistance together with declined FA β-oxidation [88,89] . In contrast, recombinant adiponectin administration exerted protective effects against NAFLD in mice [90] .…”
Non-alcoholic fatty liver disease (NAFLD) is a common health problem with a high mortality burden due to its liver-and vascular-specific complications. It is associated with obesity, high-fat diet as well as with type 2 diabetes mellitus (T2DM) and metabolic syndrome (MetS). Impaired hepatic fatty acid (FA) turnover together with insulin resistance are key players in NAFLD pathogenesis. Peroxisome proliferator-activated receptors (PPARs) are involved in lipid and glucose metabolic pathways. The novel concept is that the activation of the PPARα subunit may protect from liver steatosis. Fenofibrate, by activating PPARα, effectively improves the atherogenic lipid profile associated with T2DM and MetS. Experimental evidence suggested various protective effects of the drug against liver steatosis. Namely, fenofibraterelated PPARα activation may enhance the expression of genes promoting hepatic FA β-oxidation. Furthermore, fenofibrate reduces hepatic insulin resistance. It also inhibits the expression of inflammatory mediators involved in non-alcoholic steatohepatitis pathogenesis. These include tumor necrosis factor-α, intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1 and monocyte chemoattractant protein-1. Consequently, fenofibrate can limit hepatic macrophage infiltration. Other liver-protective effects include decreased oxidative stress and improved liver microvasculature function. Experimental studies showed that fenofibrate can limit liver steatosis associated with high-fat diet, T2DM and obesity-related insulin resistance. Few studies showed that these benefits are also relevant even in the clinical setting. However, these have certain limitations. Namely, these were uncontrolled, their sample size was small, fenofibrate was used as a part of multifactorial approach, while histological data were absent. In this context, there is a need for large prospective studies, including proper control groups and full assessment of liver histology.
“…A higher value of leptin according to E Tsochatzis can enhance IR, increase the cellular pool of fatty acids, and lead to the formation of liver steatosis [31]. B.Mattioli demonstrated that leptin may enhance the production of proinflammatory cytokines, including TNF-α [32].…”
The aim of this study was to determine the role of the most informative indicators of adipocytokine status and ghrelin in insulin resistance (IR) formation in chronic hepatitis C (CHC) patients at different stages of liver fibrosis.Materials and Methods: This study included 205 CHC patients with HCV genotypes 1 and 3. A comparative analysis of the laboratory parameters was carried out in a group of patients with IR (n=110) and without IR (n=95) and in patients depending on the stage of liver fibrosis. The serum levels of adipocytokines and ghrelin were determined using Bachem Group (USA) and Immundiagnostik AG (Germany) test systems with microplate reader Elx800 (FinBio, Finland). Diagnosis and assessment of the degree of fibrosis was performed by liver biopsy, liver elastometry and calculation test FibroTest.Results: Obtained data allow us to regard the decreased secretion of ghrelin, and increased production of leptin, resistin and TNF-α as a component involved in the formation of IR in CHC patients. (Int J Biomed. 2016;6(1):27-32.).
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