Ildiko Lingvay, Ruchi Mathur, Edward W Szczepaniak and Lidia S Szczepaniak
Aims: Type 2 diabetes is a progressive disease and highly prevalent in Hispanic and Black minorities in the United States. Our research suggested that Black, compared to Hispanic and non-Hispanic White accumulate less of triglyceride within pancreatic tissue. Herein we describe ethnicity specific aspects of the relationship between pancreatic TG levels and beta cell function.
Methods: We studied 68 women: 16 Black, 26 Hispanic and 26 non-Hispanic White. We assessed insulin secretion and insulin sensitivity using frequently sampled glucose tolerance test - FSIVGTT, abdominal fat distribution using magnetic resonance imaging - MRI, and pancreatic triglyceride levels using proton magnetic resonance spectroscopy - 1H MRS.
Results: Characteristics and results were similar for non-Hispanic White and Hispanic women, hence, we considered White and Hispanic as one group. In Hispanic/White pancreatic TGs were low in lean, elevated in obese and highest in type 2 diabetes. Beta-cell function, measured as a disposition index was lower in obese compared to lean and lowest in type 2 diabetes. Furthermore, pancreatic triglyceride (pTG) and the disposition index (DI) were inversely correlated: DI 251 660 pTG = + , R2=0.4099. In non-Hispanic Black pancreatic triglyceride content was lower than in Hispanic/White, lowest in lean and marginally elevated in obese and type 2 diabetes. Beta cell function was low/normal in lean, significantly augmented in obese and reduced in type 2 diabetes. Unlike in Hispanic/White, in Blacks beta cell function expressed by DI was linearly proportional to pTG content: DI= 328*pTG + 430, R2=0.4472.
Conclusions: The results of this research suggest an ethnicity specific relationship of beta-cell function and pTG content. In Hispanics/Whites, high pancreatic TG levels potentially represent the risk factor for beta-cell failure. In obese Blacks however, hypersensitivity of beta-cell to elevated pTGs and subsequent exaggerated glucose stimulated insulin secretion may represent the ultimate risk factor for the future advance to beta-cell failure.