Written by Chrystal Moulton, Staff Writer. This study examines the relationship between fat distribution and inflammatory markers associated with T2D in white men but not black men.

diabetesUnlike other ethnicities, African populations are at a higher risk of developing type 2 diabetes compared with white populations. This prevalence, however, cannot be explained simply by obesity or economics 1,2 . Research in diabetes has linked distribution of fat to the risk of insulin resistance 3-5. Nonetheless, it has not been shown whether this could explain the reason for the higher prevalence of type 2 diabetes among black ethnic groups versus those of white European descent.

In a cross-sectional analysis of a smaller sample of participants from the Soul Deep study 6, researchers wanted to determine the relationship between glycemic state and specific adipose tissue inflammation markers in Black West African men versus White European men. They hypothesized that measures of inflammation and visceral and deep subcutaneous adipose tissue would be stronger in Black West African men that White European men.

Sixty-five men who met the eligibility criteria were included in this study; 42 were of white European descent and 43 were of black West African descent. These members were then divided into the following groups based on glucose tolerance:

  • White European normal glucose tolerance (WE-NGT) n=23
  • White European Type 2 diabetes (WE-T2D) n=19
  • Black West African normal glucose tolerance (BWA-NGT) n=23
  • Black West African Type 2 diabetes (BWA-T2D) n=20

Researchers assessed abdominal subcutaneous adipose tissue (ASAT), deep subcutaneous adipose tissue (dSAT), superficial subcutaneous adipose tissue (sSAT), and visceral adipose tissue (VAT) through an MRI scan taken after overnight fasting. Participants who took metformin were required to stop metformin treatment 7-days prior to the scan. Blood was taken to determine inflammatory markers (IL-6, IL-8, IL-10, TNF-alpha & gamma, resistin, leptin, adiponectin, and vascular endothelial growth factor (VEGF)).

Overall, no significant ethnicity by glycemic state interaction was observed for cholesterol, triglycerides, waist circumference, BMI, age, or weight. All regional fat depots were significantly higher in men with type 2 diabetes (T2D). However, visceral adipose tissue (VAT) (p=0.002) to abdominal subcutaneous adipose tissue (ASAT) [VAT:ASAT] (p=0.002), and deep subcutaneous adipose tissue (dSAT) to superficial subcutaneous adipose tissue (sSAT) [dSAT:sSAT] (p=0.034) was significantly lower in BWA men. BWA men had significantly lower TNF-alpha (p=0.034) and adiponectin (p=0.005) and greater IL-10 (p=0.019) compared to WE men regardless of glycemic state. Significant inverse association was observed between adiponectin and sSAT in WE but for BWA men, adiponectin and sSAT were positively associated (ethnic interaction p=0.003). Furthermore, even after adjustment for age, adiponectin was inversely associated with sSAT and dSAT in WE men but not in BWA men [WE:BWA; r=-0.34, p=0.033: r=0.13, p=0.425; r=-0.31, p=0.052: r=-0.08, p=0.606, respectively]. In both BWA and WE men of NGT and T2D state, leptin was significantly associated with VAT (p≤0.05; except for BWA NGT- p=0.070), sSAT (p≤0.01), and dSAT (p≤0.018). IL-6 was significantly and positively associated with VAT in WE men and BWA men (r=0.53, p=0.001 and r=-0.34, p=0.033, respectively) but after adjustment for age, IL-6 and VAT was only significantly associated in WE NGT men (r=0.53, p=0.009). Furthermore, dSAT and IL-6 were positively correlated in WE NGT men (r=0.45, p=0.030) but not BWA men.

The study showed a significant interaction between adipose tissue distribution and inflammatory markers in WE men compared to BWA men. Furthermore, BWA men have more favorable fat distribution and thus exhibiting weaker interactions between adiposity and inflammatory makers of insulin resistance. Therefore, fat distribution and adipose tissue inflammation may not explain why BWA men are at greater risk for T2D. More studies are needed to elucidate the role of inflammatory markers on the development of T2D in black ethnic groups.

Source: Hakim, Olah, Oluwatoyosi Bello, Meera Ladwa, Janet L. Peacock, A. Margot Umpleby, Geoffrey Charles-Edwards, Stephanie A. Amiel, and Louise M. Goff. “The Link between Obesity and Inflammatory Markers in the Development of Type 2 Diabetes in Men of Black African and White European Ethnicity.” Nutrients 12, no. 12 (2020): 3796.

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Posted February 8, 2021.

Chrystal Moulton BA, PMP, is a 2008 graduate of the University of Illinois at Chicago. She graduated with a bachelor’s in psychology with a focus on premedical studies and is a licensed project manager. She currently resides in Indianapolis, IN.

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