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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
Published on: February 17, 2023
Insulin resistance in liver cirrhosis
Vedat Goral1, Roni Atalay, Mehmet Kucukoner
1Department of Gastroenterology, Dicle University, Medicine Faculty, Diyarbakir, [corrected] Turkey. vegoral@hotmail.com
Background/Aims:
Liver cirrhosis is a chronic disease by degeneration, regeneration and fibrosis in the liver parenchyma, caused by many diseases. Insulin resistance can be defined as any type of decrease in the effect that may occur at the phases following insulin's secretion from beta-cells of the pancreas, where it is produced, until it has the expected effects in the target cells. The aim of the present study is to demonstrate the presence of insulin resistance in LC, which is common in our country and region, and investigate the existence of association between insulin resistance occuring in LC and cytokine levels, age, gender, CRP, Hs-CRP, Child-Pugh score and etiology of LC.
Methodology:
A total of 79 patients with liver cirrhosis (group 1) were included in the study, and 50 subjects as controls (group 2). Of liver cirrhosis patients, 49 (62%) were male and 30 (38%) were female, with a mean age of 54.71 +/- 14.68. Of the controls, 23 (46%) were male and 27 (54%) were female, with a mean age of 41.9 +/- 11.54. Severity of cirrhosis was assessed by Modified Child-Turcoutte-Pugh score. Seven cases (8.9%) were at the Child-Pugh stage A, 35 cases (44.3%) at the Child-Pough stage B, and 37 cases (46.8%) at the Child-Pough stage C. HOMA-IR was calculated and values > 2.7 were regarded as presence of insulin resistance (HOMA-IR +). Serum glucose, albumin, bilirubin values were studied with enzymatic method (Architect C-16000); serum CRP, Hs-CRP values with nephelometric method by Beckman Coulter Image Nephelometer (immunochemistry system); insulin, C-peptide with electrochemiluminance immunological method; prothrombin time with radiation method by ACL-Advance brand device.
Results:
In this study, glucose (p = 0.004), insulin (p = 0.010), C-peptide (p < 0.001), HOMA-IR (p < 0.001), TNF-alpha (p < 0.001), IL-2RES (p < 0.001), IL-6 (p = 0.002), CRP (p < 0.001) and HsCRP (p = 0.006) levels are elevated in LC patients, compared to control group. Consequently, high HOMA-IR in LC supports the fact that insulin resistance develops in LC, as it is reported in similar studies. When HOMA-IR positive and negative patients within LC patients are compared, it is seen that insulin resistance develops independently of age, etiology, gender, Child-Pugh classification, spleen size, TNF-alpha, IL-16, IL-2RES, IL-6, IL-10, CRP, Hs-CRP (p > 0.05) levels.
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