Skip to main content
ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #150760
Title: HIGH FAT DIET INCREASES GLUCONEOGENESIS IN OBESE BUT NOT NON-OBESE ADOLESCENTS

Author
item Sunehag, Agneta
item Bier, Dennis
item Haymond, Morey

Submitted to: Pediatric Research
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2003
Publication Date: 4/1/2003
Citation: Sunehag AL, Bier DM, Haymond MW. High Fat Diet Increases Gluconeogenesis in Obese But Not Non-Obese Adolescents. Pediatr Res 2002 53:169A

Interpretive Summary: No interpretive summary required.

Technical Abstract: BACKGROUND: The incidence of obesity and type 2 diabetes in children have increased dramatically over the past two decades. We have demonstrated that in non-obese adolescents, neither glucose production (GPR) nor gluconeogenesis (GNG) are adversely affected by dietary macronutrient composition, but it is not known whether this is the case in obese adolescents. OBJECTIVE: To determine whether obesity and dietary macronutrient composition affect GPR and GNG in healthy adolescents. DESIGN/METHODS: Eight obese adolescents (6 f; 2m;14.7±0.2 y; 88.2±3.4 kg; 32.2±0.9 kg/m2; 42.3±2.0% body fat; Tanner IV-V) (mean±SE) were studied twice following (in random order) 7-d of a high carbohydrate (HCHO) (60% CHO; 25% Fat) or a high fat (HF) (30% CHO; 55% Fat) diet. The diets were isocaloric and isonitrogenous. GPR was measured using isotope dilution of [1-13C]glucose and GNG from the deuterium incorporation at glucose carbon 5 following ingestion of deuterium oxide. Effects of diet were determined by paired t-test and of obesity by comparing the results from the obese subjects with those previously obtained in non-obese adolescents (6 fm; 4 m; 14.5±0.3 y; 55.4±3.1 kg; 20.2±0.9 kg/m2; 17.2±1.4% body fat; Tanner IV-V) (J Clin Endocrinol Metab 87(11), 2002). RESULTS: When compared to non-obese adolescents, obese adolescents had higher insulin but similar glucose, resulting in higher insulin/glucose ratio (indicating insulin resistance). GPR (based on lean body weight) was unaffected by obesity and diet. Following the HCHO diet, GNG was also not different between the two groups. However, in response to the HF diet, GNG was higher in the obese subjects. CONCLUSIONS: Regardless of diet, the obese adolescents were insulin resistant but maintained normoglycemia by increasing insulin secretion. Although glucose production rates were not affected by obesity or diet, in obese adolescents, the high fat diet increased gluconeogenesis.