4.7 Article

Insulin Resistance Is Not Increased in Inflammatory Bowel Disease Patients but Is Related to Non-Alcoholic Fatty Liver Disease

Journal

JOURNAL OF CLINICAL MEDICINE
Volume 10, Issue 14, Pages -

Publisher

MDPI
DOI: 10.3390/jcm10143062

Keywords

inflammatory bowel disease; insulin resistance; nonalcoholic fatty liver disease

Funding

  1. Spanish Ministry of Health, Subdireccion General de Evaluacion y Fomento de la Investigacion, Plan Estatal de Investigacion Cientifica y Tecnica y de Innovacion
  2. Fondo Europeo de Desarrollo Regional-FEDER-(Fondo de Investigaciones Sanitarias) [FIS PI14/00394, PI17/00083]

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This study found that insulin resistance (IR) is not increased in inflammatory bowel disease (IBD) patients with low disease activity compared to controls. However, the presence of nonalcoholic fatty liver disease (NAFLD) favors the development of IR in patients with IBD.
Background. Insulin resistance (IR) has been linked to inflammatory states. The aim of this study was to determine whether IR is increased in a cohort of inflammatory bowel disease (IBD) patients with low disease activity. We additionally intended to establish which factors were the determinants of IR in this population, including the presence of nonalcoholic fatty liver disease (NAFLD). Methods. Cross-sectional study encompassing 151 IBD patients and 174 non-diabetic controls. Insulin and C-peptide serum levels and IR and beta cell function (%B) indices based on homoeostatic model assessment (HOMA2) were assessed in patients and controls. Liver stiffness as measured by transient elastography, and the presence of NAFLD detected via ultrasound were additionally assessed. A multivariable regression analysis was performed to evaluate the differences in IR indexes between patients and controls, and to determine which predictor factors were associated with IR in IBD patients. Results. Neither HOMA2-IR (beta coef. -0.26 {95%CI -0.64-0.13}, p = 0.19) nor HOMA2-%B (beta coef. 15 {95%CI -14-44}, p = 0.31) indexes differed between patients and controls after fully multivariable analysis. Among classic IR risk factors, obesity, abdominal circumference, and triglycerides significantly and positively correlated with IR indexes in IBD patients. However, most features related to IBD, such as disease patterns, disease activity, and inflammatory markers, were not associated with IR. The presence of NAFLD was independently and significantly associated with beta cell dysfunction in patients with IBD (HOMA2-B grade 4, 251 +/- 40 vs. grade 1, 107 +/- 37, p = <0.001). Conclusions. IR is not increased in IBD patients with low disease activity compared to controls. However, the presence of NAFLD favors the development of IR in patients with IBD.

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