Obesity, adipocyte hypertrophy, fasting glucose, and resistin are potential contributors to nonalcoholic fatty liver disease in South Asian women

Figures

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  Figure 1. Anthropometric measures in participants with varying degree of nonalcoholic fatty liver (NAFL). (A) Participants with higher grade of fatty liver had a significantly higher waist circumference (WC). Post-hoc analyses indicate a significant increase in WC between each grade of NAFL. (B) Participants with fatty liver had a significantly higher body mass index (BMI) as shown by post-hoc analyses, which indicate a significant increase in BMI between NAFL 0 and NAFL 1, but not between NAFL 1 and NAFL 2. (C) Participants with fatty liver had a significantly higher hip circumference as shown by post-hoc analyses, which indicate a significant increase in hip circumference between NAFL 0 and NAFL 1, but not between NAFL 1 and NAFL 2. (D) Waist-to-hip ratio was not significantly different among fatty liver grade. Hepatic steatosis was assessed using ultrasound. n=10–13 per group. ANOVA with Bonferroni–Holm corrections analyses was performed.

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  Figure 2. Mean adipocyte size in participants with varying degree of nonalcoholic fatty liver (NAFL). (A) Participants with NAFL 2 had a significantly higher abdominal adipocyte area as shown by post-hoc analyses, which also indicate increases in abdominal adipocyte area between NAFL 0 and NAFL 1 and NAFL 1 and NAFL 2 that are trending significance. (B) Representative H&E-stained sections of abdominal adipose tissue (subcutaneous) are shown for each group. (C) Participants with fatty liver had a significantly higher omental (visceral) adipocyte area as shown by post-hoc analyses, which indicate a significant increase in adipocyte area between NAFL 0 and NAFL 1, but not between NAFL 1 and NAFL 2. Hepatic steatosis was assessed using ultrasound. Adipocyte area was measured using the ImageJ software. n=10–13 per group. ANOVA with Bonferroni–Holm corrections analyses was performed.

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  Figure 3. Elevated fasting blood glucose with degree of nonalcoholic fatty liver (NAFL). Participants with fatty liver had significantly higher fasting blood glucose (FBG) as shown by post-hoc analyses, which indicate a significant increase in FBG between NAFL 0 and NAFL 1, but not between NAFL 1 and NAFL 2. Hepatic steatosis was assessed using ultrasound. n=10–13 per group. ANOVA with Bonferroni–Holm corrections analyses was performed.

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  Figure 4. Elevated resistin associated with nonalcoholic fatty liver (NAFL) grade 2. Participants with fatty liver had serum resistin values that were trending significance. Participants with NAFL 2 had a significantly higher serum resistin as shown by post-hoc analyses, which also indicate increases in serum resistin between NAFL 1 and NAFL 2. No difference was found between NAFL 0 and NAFL 1. Hepatic steatosis was assessed using ultrasound. n=10–13 per group. ANOVA with Bonferroni–Holm corrections analyses was performed.