Decrease in fasting insulin secretory function correlates with significant liver fibrosis in Japanese non‐alcoholic fatty liver disease patients

Abstract

Background and Aim: Non-alcoholic fatty liver disease (NAFLD) is typically associated with metabolic syndrome and diabetes, and insulin resistance is involved in its pathogenesis. However, the relationship between insulin secretion and NAFLD is unclear. We aimed to characterize the relationship between fasting insulin secretory function (ISF), evaluated using the homeostatic model assessment-beta cell function (HOMA-β) and the severity of fibrosis during NAFLD. Methods: A-β was calculated in 188 patients with biopsy-confirmed NAFLD, and the correlations between Log HOMA-β and clinical parameters, including hepatic fibrosis, were calculated. Results: Log HOMA-β was significantly lower in NAFLD patients with significant fibrosis (stages 2-4) than in those in the early stages (stages 0-1) (median [interquartile range]) (2.1 [1.9-2.4] vs 2.0 [1.8-2.2], P = 0.04). The prevalence of significant fibrosis decreased with increasing Log HOMA-β: it was 59.2% in participants with low ISF (Log HOMA-β < 1.85), 43.6% in those with intermediate ISF (1.85 ≤ Log HOMA-β < 2.25), and 68.0% in those with high ISF (Log HOMAβ ≥ 2.25). Patients with lower Log HOMA-β had lower current body mass index (BMI), BMI at 20 years of age, and peak lifetime BMI than patients with intermediate or high Log HOMA-β. Conclusions: Fasting ISF decreased alongside the development of liver fibrosis in NAFLD, suggesting that an impaired β cell function has a characteristic finding of significant liver fibrosis in relatively nonobese Japanese patients.

Exploration of new therapeutic targets for viral hepatic fibrosis, alcoholic hepatic fibrosis, and non-alcoholic hepatic fibrosis

“…Diabetic patients are also usually obese and have nonalcoholic hepatic fibrosis (27). Japanese scholars have found that fasting insulin secretion could decrease with the process of non-alcoholic hepatic fibrosis (28), which may be related to glucose metabolism disorder and lipid metabolism disorder caused by islet β cell dysfunction (29). Moreover, advanced HCV hepatic fibrosis is associated with insulin resistance (30).…”

Pancreatic β-Cell Dysfunction Is Associated with Nonalcoholic Fatty Liver Disease

“…One study in Italy demonstrated β-cell function is lowered in biopsyproven NASH patients, but not in simple steatosis subjects [18]. Norimasa et al found that in NAFLD patients, HOMA-B% was decreased with the severity of liver fibrosis [19]. However, another study in the US found that HOMA-B% was remarkably higher in NAFLD participants and in those with β-cell dysfunction, even in simple steatosis patients [20].…”

Pretransplant HOMA-β Is Predictive of Insulin Independence in 7 Patients With Chronic Pancreatitis Undergoing Islet Autotransplantation

“…26 Normal β-cell function has HOMA-β scores 60%−100% 27 ; scores <40 are considered clinically dysfunctional, 18 and those >100% indicate overwork. 28 The SUITO index determines endogenous insulin secretion in T1D patients requiring insulin injection, by FCP (ng/mL)/ (FPG−63 [mg/dL]) × 1500, with values ≥26 reportedly correlating with insulin independence. 18 The BETA-2 score 19 is updated from the BETA score, 29 quantitated by ((√FCP (nmol/L) × (1−total daily insulin dose units/kg))/((FPG (mmol/L) x HbA1c (%)) within the range of 0−42; scores ≥16.2 reportedly correlate with insulin independence in T1D 19 and PIAT 20 patients.…”