Page Banner

United States Department of Agriculture

Agricultural Research Service


item Kaplan, Walid
item Sunehag, Agneta
item Dao, Harry
item Haymond, Morey

Submitted to: Diabetes
Publication Type: Abstract Only
Publication Acceptance Date: 2/23/2003
Publication Date: 5/1/2003
Citation: Kaplan W, Sunehag AL,Dao H, Haymond MW. Effects of Feeding and rhGH on Gluconeogenesis in Humans. 2003 Diabetes 52:A340.

Interpretive Summary: No interpretive summary required.

Technical Abstract: A number of factors are thought to increase the rate of gluconeogenesis (GNG) such as prolonged fasting and hormonal factors (e.g. growth hormone, insulin deficiency and glucocorticoids). Recent data from our laboratory demonstrate that GNG is not suppressed during feeding when compared to short term fasting. To determine the effect of short term rhGH on GNG under feeding and fasting conditions, six (6) healthy volunteers (23.5±6 yr, 61.3±7.6 kg, 161.6±7.3 cm and 23.6±2.5 kg/m2) were studied on two separate occasions. Subjects received, in random order, either subcutaneous injections of normal saline (NS) or recombinant human growth hormone (rhGH), (0.05 mg/kg per day) for 7 days. Rate of glucose appearance (Ra) and GNG were measured using [U-13C]glucose MIDA following 14h fasting, and following 8h of feeding with Boost High Protein (34g every 15 minutes). Results:GNG was significantly higher during feeding than fasting in the presence or absence of rhGH, despite significant and prolonged hyperinsulinemia. No significant differences were observed in the GNG following rhGH injection when compared to saline in either the feeding or fasting conditions. In summary, GNG increases during feeding, and rhGH does not acutely affect GNG. Conclusion: Using [U-13C]glucose MIDA in human: 1) GNG is not acutely under the control of either insulin or rhGH. 2) Feeding a mixed macronutrient diet increases GNG, thus 3) The only mechanism to decrease glucose production is via decreased glycogenolysis.

Last Modified: 06/24/2017
Footer Content Back to Top of Page