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Obesity, Visceral Fat, and Poor Glycemic Control Stimulate Gluconeogenic Flux
Obesity, Visceral Fat, and Poor Glycemic Control Stimulate Gluconeogenic Flux -- Posted by Gumbo on 10-23-04 05:51
Obesity, Visceral Fat, and Poor Glycemic Control Stimulate Gluconeogenic
Flux
Obesity, visceral fat accumulation, and poorly controlled diabetes stimulate
gluconeogenic flux.
"The contribution of increased gluconeogenesis (GNG) to the excessive rate
of endogenous glucose production (EGP) in type 2 diabetes (T2DM) is well
established. However, the separate effects of obesity (total body fat),
visceral adiposity, and T2DM have not been investigated. We measured GNG (by
the (2H2O) technique) and EGP (with 3-3H-glucose) after an overnight fast in
44 type 2 diabetic and 29 gender/ethnic-matched controls," researchers in
Italy and the United States report.
"Subjects were classified as obese (body mass index 30 kg/m2 or greater) or
non obese (body mass index 2); diabetic subjects were further subdivided
according to the severity of fasting hyperglycemia [fasting plasma glucose
(FPG) <9 mM or greater than or equal to 9 mM]. EGP was similar in
nondiabetic controls and T2DM with FPG less than 9 mM but was increased in
T2DM with FPG greater than or equal to 9 mM (p<0.001)," said Amalia
Gastaldelli and collaborators at the University of Texas in the U.S. and the
University of Pisa in Italy. "Within the diabetic groups, obesity had an
independent effect to further increase basal EGP (p<0.01). In both non obese
diabetic groups, both the percent GNG and gluconeogenic flux were increased,
compared with non obese nondiabetic controls."
"In both diabetic groups, obesity further increased both percent GNG and
gluconeogenic flux," reported the investigators. "In obese and non obese
T2DM, the increase in gluconeogenic flux was not accompanied by a reciprocal
decrease in glycogenolysis, indicating a loss of hepatic autoregulation. By
multivariate analysis, gluconeogenic flux was positively correlated with
percent body fat, visceral fat, and the fasting plasma free fatty acid and
glucose concentrations (all less than or equal to 0.02)."
"We conclude that obesity per se, and visceral fat accumulation in
particular, as well as poorly controlled diabetes are potent stimuli to
augment gluconeogenic flux," stated the scientists.
Gastaldelli and associates published their study in the Journal of Clinical
Endocrinology and Metabolism (Separate contribution of diabetes, total fat
mass, and fat topography to glucose production, gluconeogenesis, and
glycogenolysis. J Clin Endocrinol Metab, 2004;89(8):3914-3921).
For additional information, contact Ralph A. DeFronzo, University of Texas
Health Sciences Center, Diabetes Division, 7703 Floyd Curl Drive MS 7886,
San Antonio, TX 78229, USA. E-mail: albarado@uthscsa.edu.
Publisher contact information for the Journal of Clinical Endocrinology and
Metabolism is: Endocrine Society, 8401 Connecticut Avenue, Suite 900, Chevy
Chase, MD 20815-5817, USA.
The information in this article comes under the major subject areas of
Obesity and Diabetes, Obesity Pathogenesis, Diabetes Pathogenesis, Type 2
Diabetes, and Endocrinology. This article was prepared by Biotech Week
editors from staff and other reports
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