Relationship of Intramyocellular Lipid to Insulin Sensitivity May Differ With Ethnicity in Healthy Girls and Women

Abstract

The prevalence of type 2 diabetes is greater among African Americans (AA) vs. European Americans (EA), independent of obesity and lifestyle. We tested the hypothesis that intramyocellular lipid (IMCL) or extramycellular lipid (EMCL) would be associated with insulin sensitivity among healthy young women, and that the associations would differ with ethnic background. We also explored the hypothesis that adipokines and estradiol would be associated with muscle lipid content. Participants were 57 healthy, normoglycemic, women and girls mean age 26 (±10) years; mean BMI 27.3 (±4.8) kg/m2; 32 AA, 25 EA. Soleus IMCL and EMCL were assessed with 1H magnetic resonance spectroscopy (MRS); insulin sensitivity with an insulin-modified frequently sampled intravenous glucose tolerance test and minimal modeling; body composition with dual-energy X-ray absorptiometry; and intra-abdominal adipose tissue (IAAT) with computed tomography. Adiponectin, leptin, and estradiol were assessed in fasting sera. Analyses indicated that EMCL, but not IMCL, was greater in AA vs. EA (2.55 ± 0.16 vs. 1.98 ± 0.18 arbitrary units, respectively, P < 0.05; adjusted for total body fat). IMCL was associated with insulin sensitivity in EA (r = −0.54, P < 0.05, adjusted for total fat, IAAT, and age), but not AA (r = 0.16, P = 0.424). IMCL was inversely associated with adiponectin (r = −0.31, P < 0.05, adjusted for ethnicity, age, total fat, and IAAT). In conclusion, IMCL was a significant determinant of insulin sensitivity among healthy, young, EA but not AA women. Further research is needed to determine whether the component lipids of IMCL (e.g., diacylglycerol (DAG) or ceramide) are associated with insulin sensitivity in an ethnicity-specific manner.

Race/Ethnicity Disparities in Dysglycemia Among U.S. Women of Childbearing Age Found Mainly in the Nonoverweight/Nonobese

“…One possible explanation for the disparity within nonobese subjects is a differential β-cell function between race/ethnicity groups. Results from clinical studies have shown decreased insulin sensitivity in African American women compared with European American women (28,29), with differential responses by race/ethnicity in insulin sensitivity and β-cell responsiveness according to level of body fat (30) and location of body fat depots (31,32). Although obesity alone causes a state of insulin resistance, it is possible that the pancreatic response is different in the presence of adipose tissue within different race/ethnicity groups, which may help to explain our observation by BMI category.…”

The Role of Adipose Tissue in Insulin Resistance in Women of African Ancestry

“…However, when MRS has been used to quantify both intramyocellular (IMCL) and extramyocellular lipid (IMCL) content, only EMCL [81], and not IMCL [56, 81], was increased in African American and black South Africans (Goedecke et al, unpublished). Further, IMCL was associated with insulin sensitivity in white, but not black women and girls [81]. …”

Effects of an overnight intravenous lipid infusion on intramyocellular lipid content and insulin sensitivity in African–American versus Caucasian adolescents

“…Lipid accumulation within muscle cells (intramyocellular lipid, IMCL) is associated with insulin resistance in obesity and T2DM [2–4]. Racial differences in insulin sensitivity have been noted in adults [5, 6] and children [7, 8], such that African-Americans have lower insulin sensitivity than their Caucasian peers despite similar BMI or total fat. IMCL is an ectopic fat depot that may in part explain the racial differences in insulin sensitivity.…”