TY - JOUR
T1 - Hyperinsulinemia in obesity
T2 - Lack of relation to gastric emptying of glucose solution or to plasma somatostatin levels
AU - Sasaki, Haruka
AU - Nagulesparan, Murugasu
AU - Dubois, André
AU - Vasquez, Barbara
AU - Johnson, Ginger C.
AU - Sievers, Maurice L.
AU - Unger, Roger H
N1 - Funding Information:
From the Human Diabetes Study Center, University of Texas Southwestern Medical School, Phoenix, Ark. and the Phoenix Clinical Research Section. National Institute of Arthritis, Diabetes. Digestive and Kidney Diseases, Phoenix, Ark. Receivefdo r publication March 18, 1983. Supported in part by NIH Research Contraci NO-I-AM-6-2219. Address reprint requests io M. Nagulesparan. M.R.C.P., Phoenix Clinical Research Section, NIH. 4212 North 16th Street. Phoenix, AZ 85016. 0026-0495/83/3207-OOlO$I .00/O
PY - 1983/7
Y1 - 1983/7
N2 - To investigate some factors that may be related to the hyperinsulinemia of obesity, we measured fractional gastric emptying rates and changes of circulating levels of glucose, insulin, and somatostatin-like immunoreactivity (SLI) following the intragastric instillation of glucose in age-matched obese and nonobese Pima Indians with normal glucose tolerance. Results for the nonobese Pimas were also compared with findings for age- and weight-matched Caucasians with normal glucose tolerance. The levels of fasting plasma insulin and the integrated insulin response to glucose were significantly greater (P < 0.01) in obese than in nonobese Pimas. Mean rates of fractional gastric emptying, both in the basal state and after the glucose load, were similar for the three groups. The fractional gastric emptying rates after a glucose load were strongly correlated with the integrated responses of both plasma glucose and insulin in the nonobese Caucasians (r = 0.88, 0.90; P < 0.01) but not in either Pima group. There were no significant differences in peripheral plasma SLI for any of the three groups, either in the basal state or after the glucose load. These findings suggest that the hyperinsulinemia of established obesity is not mediated by alterations in the gastric emptying rate of liquids or by peripheral plasma SLI concentrations. They do not, however, exclude defects in gastric emptying of solid foods. Nor do they exclude the possibility that gastric or D-cell abnormalities exist during the period of fat accumulation but recede after obesity is established.
AB - To investigate some factors that may be related to the hyperinsulinemia of obesity, we measured fractional gastric emptying rates and changes of circulating levels of glucose, insulin, and somatostatin-like immunoreactivity (SLI) following the intragastric instillation of glucose in age-matched obese and nonobese Pima Indians with normal glucose tolerance. Results for the nonobese Pimas were also compared with findings for age- and weight-matched Caucasians with normal glucose tolerance. The levels of fasting plasma insulin and the integrated insulin response to glucose were significantly greater (P < 0.01) in obese than in nonobese Pimas. Mean rates of fractional gastric emptying, both in the basal state and after the glucose load, were similar for the three groups. The fractional gastric emptying rates after a glucose load were strongly correlated with the integrated responses of both plasma glucose and insulin in the nonobese Caucasians (r = 0.88, 0.90; P < 0.01) but not in either Pima group. There were no significant differences in peripheral plasma SLI for any of the three groups, either in the basal state or after the glucose load. These findings suggest that the hyperinsulinemia of established obesity is not mediated by alterations in the gastric emptying rate of liquids or by peripheral plasma SLI concentrations. They do not, however, exclude defects in gastric emptying of solid foods. Nor do they exclude the possibility that gastric or D-cell abnormalities exist during the period of fat accumulation but recede after obesity is established.
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U2 - 10.1016/0026-0495(83)90127-0
DO - 10.1016/0026-0495(83)90127-0
M3 - Article
C2 - 6135135
AN - SCOPUS:0020640283
SN - 0026-0495
VL - 32
SP - 701
EP - 705
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 7
ER -