Abstract
Diabetes mellitus (DM) and alcohol consumption is still one of the important research models that simulate variable clinical conditions and metabolic diseases, such as alcoholic liver diseases. The aim of this study was to evaluate the long-term cumulative effects of low alcohol consumption on the liver tissue, biochemical assays and some inflammatory cytokines in experimentally-induced DM rats. Ethanol was administered in the drinking water (3% v/v) for 30 days to adult male Sprague-Dawley rats, with or without DM induced by streptozocin injection. Histological and biochemical parameters as well as some inflammatory cytokines - interleukin (IL)-4, IL-6, IL-10, and tumor necrosis factor alpha (TNF-α) - were measured. A significant increase in blood glucose level in the combination group was accompanied by a significant decrease in plasma insulin (p < 0.001 vs controls). Hepatic histopathology of the combination group revealed steatosis and fibrosis in addition to a significant increase in the gamma-glutamyltransferase (γ-GT) and alkaline phosphatase (ALP) levels (p < 0.05 and p < 0.001, respectively). A non-high-density lipoprotein (HDL) lipid profile (total cholesterol (TC), triglycerides (TG) and low-density lipoprotein (LDL)) revealed a significant increase in comparison to controls (p < 0.05), while HDL showed no significant change. The IL-4 and IL-6 levels were significantly higher (p < 0.05), while IL-10 and TNF-α revealed non-significant changes. Depletion of the hyperglycemic response in the case of low alcohol consumption in DM rats was associated with elevated plasma cytokines, especially IL-6 and IL-4, which could be a part of a host defense mechanism to repair the hepatic and pancreatic damage through this inflammatory process. The severe liver damage under insult of low alcohol consumption and DM could serve as inhibitory factors in gluconeogenesis and glycogenolysis, with little or no impact on insulin levels.
Highlights
Diabetes mellitus (DM) is a public health problem which has reached epidemic proportions worldwide.[1]
Depletion of the hyperglycemic response in the case of low alcohol consumption in DM rats was associated with elevated plasma cytokines, especially IL-6 and IL-4, which could be a part of a host defense mechanism to repair the hepatic and pancreatic damage through this inflammatory process
The severe liver damage under insult of low alcohol consumption and DM could serve as inhibitory factors in gluconeogenesis and glycogenolysis, with little or no impact on insulin levels
Summary
Diabetes mellitus (DM) is a public health problem which has reached epidemic proportions worldwide.[1]. Recent studies have shown that moderate alcohol intake is associated with changes in the levels of several cytokines, especially pro-inflammatory ones – interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α) – in different physiological and pathological states.[10]. Interleukin-6 protects against alcoholic liver injury via the activation of the signal transducer and activator of transcription 3 (STAT3), regulating liver fibrosis and inflammation, and promoting liver regeneration,while IL-10 inhibits alcoholic liver inflammation via the activation of STAT3 in Kupffer cells/macrophages (targeting immune cells) and the subsequent inhibition of liver inflammation.[11,12] Recent studies have suggested that IL-10 may play a dual role in controlling ethanol-induced steatosis and liver injury via the inhibition of pro-inflammatory cytokines, such as TNF-α, thereby decreasing alcoholic liver injury, or via the inhibition of the hepatoprotective cytokine IL-6, thereby potentiating alcoholic liver injury.[13]. Diabetes mellitus (DM) and alcohol consumption is still one of the important research models that simulate variable clinical conditions and metabolic diseases, such as alcoholic liver diseases
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