Abstract P234: High Sodium Intake is Associated with Increased Hemoglobin A1C in Young Overweight/Obese African Americans
Introduction: Whether high sodium intake, assessed by 24-hour urinary sodium excretion (24hrUNaEx), is associated with altered glycemic control, evaluated by hemoglobin A1C (HbA1C), in the African American population remains unknown. We aimed to evaluate the relationship between 24hrUNaEx and HbA1C in young overweight/obese African Americans.
Methods: A total of 106 apparently healthy overweight/obese drug-naïve African Americans were recruited. Subjects were asked to discard the first morning urine specimen and collect all remaining urine specimens for next 24-hr including a urine specimen of the following morning. HbA1C was measured from venous blood by ion-exchange chromatography.
Results: The means (± SE) of age and body mass index (BMI) of subjects (67%, 71/106 females) were 24.30±0.82 years and 35.51±0.70 kg/m2, respectively. Average 24hrUNaEx was 172.17±7.09 mEq/L/d, which corresponded to average sodium intake of 3.96±1.63 g/d. Pearson’s correlation analysis revealed a positive correlation between log transformed 24hrUNaEx and HbA1C after adjusting for age, sex, BMI, and systolic blood pressure (r=0.20, p=0.04). In a subgroup analysis involving subjects with HbA1C ≥5.7% (N=40), the correlation between 24hrUNaEx and HbA1C was stronger even with adjustment for the above variables (r=0.35, p=0.04).
Conclusions: High sodium intake is associated with increased HbA1C independent of traditional risk factors in our study population. This relationship was stronger in subjects with HbA1C ≥5.7%, which by definition represents prediabetes (HbA1C ≥5.7 & <6.5%) and diabetes (HbA1C ≥6.5%). Although not fully understood, the possible mechanism by which high sodium intake could contribute to glycemic dysregulation involves cellular dysfunction and apoptosis of pancreatic beta cell induced by high sodium intakes via inflammation and oxidative stress.
Author Disclosures: S.J. Parikh: None. J. Bhagatwala: None. A. Raed: None. Y. Huang: None. I. Kotak: None. G.A. Harshfield: None. Y. Dong: None. H. Zhu: None.
This research has received full or partial funding support from the American Heart Association, Greater Southeast Affiliate (Alabama, Florida, Georgia, Louisiana, Mississippi, Puerto Rico & Tennessee).
- © 2015 by American Heart Association, Inc.