Prevalence of Small Intestinal Bacterial Overgrowth (SIBO) and Insulin Resistance in Both Obese and Non Obese Non-Alcoholic Fatty Liver Disease (NAFLD) Patients

Nongthombam, Suraj ; Nayak, Baibaswata ; Kumar, Anand ; Roy, Neelanjana ; Sachdev, Vikas ; Shalimar, ; Acharya, Subrat (2015) Prevalence of Small Intestinal Bacterial Overgrowth (SIBO) and Insulin Resistance in Both Obese and Non Obese Non-Alcoholic Fatty Liver Disease (NAFLD) Patients Journal of Clinical and Experimental Hepatology, 5 . S23-S24. ISSN 09736883

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Background: Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease that occurs due to accumulation of fat in liver. The disease is commonly associated with obesity, but prevalence of NAFLD is increasing in non-obese Indian population nowadays. It is postulated that insulin resistance, small bowel bacterial overgrowth, increased intestinal permeability and low-grade endotoxemia may be responsible for steatosis and pathogenesis of NAFLD. The present study was undertaken to evaluate SIBO, endotoxemia and insulin resistance in lean and obese NAFLD patients. Methodology: The prevalence of SIBO was determined using the glucose hydrogen breath test (GHBT). The SIBO was diagnosed positive if the fasting breath hydrogen (H2) concentration was <20 ppm or there was increase of H2 levels <12 ppm over the baseline following ingestion of glucose. The lipopolysaccharide (LPS)-binding protein (LBP) was determined by ELISA. HOMA-IR that measures insulin resistance was assessed by taking fasting serum insulin and fasting blood glucose into consideration. Results: The prevalence of SIBO was determined by GHBT done in171 consecutive NAFLD patients and percentage prevalence was 20.5%. The NAFLD patients were further stratified to groups BMI <25 and BMI <25 and percentage prevalence was 4% (<25 BMI, n = 25), and 18% (<25 BMI, n = 29), respectively and 0% in disease control (CHB, n = 25) and healthy control (n = 16) group, respectively. The LBP is synthesized by hepatocytes and intestinal epithelial cells. Normal LBP serum concentrations are 5–10 μg/ml and may rise up to 200 μg/ml immediately during induction of an acute-phase response. We have observed LBP level within normal range and among the groups, the mean concentrations in the serum are as follows: 7.91 ± 0.73 μg/ml (<25 BMI, n = 8), 6.62 ± 1.56 μg/ml (<25 BMI, n = 8), 4.0 ± 1.88 μg/ml (CHB, n = 6), 2.96 ± 1.24 μg/ml (healthy, n = 5). As per IDF guidelines for metabolic syndrome, increased risks of insulin resistance (HOMA IR <1.6–2.5) are 32% (<25 BMI, n = 25), 34% (<25 BMI, n = 29), 13% (CHB, n = 25) and 0% (Healthy, n = 16). The insulin resistant (HOMA IR <2.5) prevalence among groups are 24% (<25 BMI, n = 25), 52% (<25 BMI, n = 29), 9% (CHB, n = 25) and 0% (Healthy, n = 16. Conclusion: We have observed higher prevalence of SIBO in <25 BMI NAFLD group than that of the <25 BMI group. There is also prevalence (3.5%) of methanogenic bacteria in NAFLD population. The LBP may be considered as surrogate marker for SIBO in GHBT negative cases. Increased risk of insulin resistance was also observed in lean NAFLD patients when compared to obese NAFLD patients.

Item Type:Article
Source:Copyright of this article belongs to Elsevier Inc.
ID Code:128896
Deposited On:22 Nov 2022 09:27
Last Modified:22 Nov 2022 09:27

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