Plasma Epinephrine Predicts Fasting Glucose in Centrally Obese African-American Women

被引:9
|
作者
Surwit, Richard S. [1 ]
Williams, Redford B. [1 ]
Lane, James D. [1 ]
Feinglos, Mark N. [1 ]
Kuhn, Cynthia M. [2 ]
Georgiades, Anastasia [1 ]
机构
[1] Duke Univ, Sch Med, Dept Psychiat & Behav Sci, Durham, NC 27706 USA
[2] Duke Univ, Sch Med, Dept Pharmacol & Canc Biol, Durham, NC USA
关键词
ADIPOSE-TISSUE; FAT DISTRIBUTION; ABDOMINAL FAT; MINIMAL MODEL; RISK-FACTORS; STRESS; ATHEROSCLEROSIS; METABOLISM; ADULTS;
D O I
10.1038/oby.2010.43
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The high prevalence of diabetes in African-American (AA) women has been widely assumed to be related to the greater prevalence of obesity in this group. Catecholamine release acting on central adipose tissue has been proposed to be a contributing factor. The aim of this article was to examine the interaction of plasma catecholamines and central adiposity on fasting and nonfasting glucose levels in two separate samples. In both studies, the women were healthy, nondiabetic of similar age. In addition, both studies assessed plasma epinephrine (EPI) and norepinephrine (NOREPI) levels collected at three time points. In study 1, catecholamines were measured during a standardized laboratory mental stress task and in study 2, they were measured during the initial phase (10 min) of an intravenous glucose tolerance test (IVGTT). Results from both studies revealed significant effects of EPI on fasting glucose in the obese women. In study 1, mean EPI levels were significantly related to fasting glucose in AA women with high trunk fat (beta = 0.60, P < 0.001). Because high BMI was associated with high trunk fat in women, we used BMI >30 as a proxy for high trunk fat (>32%) in study 2. In study 2, EPI response to the glucose bolus was a strong predictor of fasting glucose in AA women with BMI >30 (beta= 0.75, P < 0.003). We conclude that the effect of central adiposity on fasting glucose may be moderated by plasma EPI. This suggests that adrenal medullary activity could play a role in the pathophysiology of type 2 diabetes.
引用
收藏
页码:1683 / 1687
页数:5
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