TY - JOUR
T1 - Insulin resistance in adipocytes of obese women
T2 - Effects of body fat distribution and race
AU - Dowling, Hillary J.
AU - Fried, Susan K.
AU - Pi-Sunyer, F. Xavier
N1 - Funding Information:
From the Obesity Research Center, Department of Medicine, St. Luke's/Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, NY; and Department of Nutritional Sciences, Cook College, Rutgers University, New Brunswick, NJ. Submitted May 26, 1994; accepted October31, 1994. Supported by grants from the National Institutes of Health (DK-40414 and 5T32-DK-07559-02) and the Weight Watchers Foundation. Address reprint requests to F. Xavier Pi-Sunyer, MD, Director, Obesity Research Center, St. Luke's/Roosevelt Hospital Center, Woman's Hospital, lOth Floor, Amsterdam Avenue at ll4th Street, New York, NY lO025. Copyright © 1995 by W.B. Saunders Company 0026-0495/95/4408-0005503.00/0
PY - 1995/8
Y1 - 1995/8
N2 - Upper-body obesity (UBO) in white women is associated with increased fatty acid turnover and resistance to the effects of insulin on systemic glucose metabolism. The present study determined whether the abilities of insulin to stimulate glucose transport and suppress lipolysis are impaired in adipocytes from white UBO (W-UBO) women. Because the clinical risks associated with UBO are attenuated in black women, the effects of race on adipocyte insulin sensitivity were assessed. Forty-two healthy, equally obese women were selected for study on the basis of race (black or white) and body fat distribution (UBO or lower-body obesity [LBO]). In white women, both abdominal and gluteal fat cells from the UBO versus LBO group were less responsive to the stimulatory effects of insulin on glucose uptake and less sensitive to the antilipolytic effects of insulin and the adenosine analog, phenylisopropyladenosine (PIA). In contrast, in black women, fat cells from UBO and LBO groups were equally sensitive to the stimulatory effects of insulin on glucose transport and the suppressive effects of insulin and PIA on lipolysis. These in vitro data correlate well with previous clinical findings that UBO in white women but not in black women is associated with insulin resistance and dyslipidemia. Thus, resistance to the antilipolytic effects of insulin and adenosine at the level of adipose tissue may increase systemic lipolysis and play a role in the development or maintenance of peripheral insulin resistance associated with UBO in white women, but not in black women.
AB - Upper-body obesity (UBO) in white women is associated with increased fatty acid turnover and resistance to the effects of insulin on systemic glucose metabolism. The present study determined whether the abilities of insulin to stimulate glucose transport and suppress lipolysis are impaired in adipocytes from white UBO (W-UBO) women. Because the clinical risks associated with UBO are attenuated in black women, the effects of race on adipocyte insulin sensitivity were assessed. Forty-two healthy, equally obese women were selected for study on the basis of race (black or white) and body fat distribution (UBO or lower-body obesity [LBO]). In white women, both abdominal and gluteal fat cells from the UBO versus LBO group were less responsive to the stimulatory effects of insulin on glucose uptake and less sensitive to the antilipolytic effects of insulin and the adenosine analog, phenylisopropyladenosine (PIA). In contrast, in black women, fat cells from UBO and LBO groups were equally sensitive to the stimulatory effects of insulin on glucose transport and the suppressive effects of insulin and PIA on lipolysis. These in vitro data correlate well with previous clinical findings that UBO in white women but not in black women is associated with insulin resistance and dyslipidemia. Thus, resistance to the antilipolytic effects of insulin and adenosine at the level of adipose tissue may increase systemic lipolysis and play a role in the development or maintenance of peripheral insulin resistance associated with UBO in white women, but not in black women.
UR - http://www.scopus.com/inward/record.url?scp=0029086163&partnerID=8YFLogxK
U2 - 10.1016/0026-0495(95)90094-2
DO - 10.1016/0026-0495(95)90094-2
M3 - Article
C2 - 7637656
AN - SCOPUS:0029086163
SN - 0026-0495
VL - 44
SP - 987
EP - 995
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 8
ER -