Failure of nocturnal changes in growth hormone to alter carbohydrate tolerance the following morning

Nielsen, Michael Festersen; Dinneen, Séan F.; Basu, Ananda; Basu, Rita; Alzaid, Aus; Rizza, R.

doi:10.1007/s001250051031

Cited by 10 publications

(8 citation statements)

References 47 publications

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“…Resistance to insulin includes resistance to the antilipolytic effect of insulin, and, therefore, increased insulin sensitivity might be expected to reduce lipolysis. However, further complexity is added by the recent observation that inhibition of lipolysis by acipimox abolishes the effect of GH to increase insulin resistance, suggesting that stimulation of lipolysis by GH might explain its effect on insulin sensitivity (35). Therefore, the relationship among GH, insulin, and FFA remains extremely complex and requires further investigation.…”

Section: Discussionmentioning

confidence: 95%

Effect of Growth Hormone (GH) on Glycerol and Free Fatty Acid Metabolism during Exhaustive Exercise in GH-Deficient Adults

Gibney

Healy

Stolinski

et al. 2003

The Journal of Clinical Endocrinology & Metabolism

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GH is an important regulator of fat metabolism at rest, but it is not known whether it regulates fat metabolism during exercise. To determine whether physiologic concentrations of GH influence fat metabolism during exercise, we randomized 16 GH-deficient adults, receiving long-term (mean duration, 5 yr) GH replacement, to either continue GH (n = 8) or receive identical placebo (n = 8) for a 3-month period. Metabolic studies, at rest, during and following exhaustive exercise were carried out at baseline and at the end of the 3 months. The rate of appearance of glycerol (glycerol Ra, an index of lipolysis) and free fatty acids (FFA, FFA Ra) and the rate of disappearance of FFA (FFA Rd) in the plasma were measured using infusions of (2)H(5)-glycerol and 1-(13)C-palmitic acid. Changes in body composition were assessed using dual-energy x-ray absorptiometry scanning and anthropometric measurements. In the baseline studies, exercise resulted in an increase in plasma glycerol and FFA concentrations, glycerol Ra, FFA Ra, and FFA Rd (P < 0.001). Three months of GH withdrawal resulted in reductions in plasma glycerol and FFA, glycerol Ra, FFA Ra, and FFA Rd at rest (P < 0.05 vs. baseline) and during exercise (P < 0.05 vs. baseline and vs. GH treated). Lean body mass decreased after 3 months of GH withdrawal, but total body fat, trunk fat, waist circumference, and the sum of skinfold thicknesses increased after 3 months of GH withdrawal (P < 0.05 vs. baseline and vs. GH treated). Fasting insulin and homeostasis model assessment of insulin resistance decreased after 3 months of GH withdrawal (P < 0.05 vs. baseline and vs. GH treated). In summary, GH withdrawal for 3 months resulted in reductions in release of glycerol and FFA into the circulation and uptake of FFA into the tissues during intense exercise. These changes were accompanied by reduced lean body mass and increased total body and trunk fat. Further studies are required to determine whether reduced mobilization of fat during exercise contributes to reduced exercise capacity and increased body fat in GH-deficient adults.

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Section: Discussionmentioning

confidence: 95%

Effect of Growth Hormone (GH) on Glycerol and Free Fatty Acid Metabolism during Exhaustive Exercise in GH-Deficient Adults

Gibney

Healy

Stolinski

et al. 2003

The Journal of Clinical Endocrinology & Metabolism

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“…In humans, no dose-ranging studies have been reported, but in nondiabetic subjects after evening ethanol intake of 0.8Ϫ1.5 g/kg, a more than two-thirds reduction in integrated response of growth hormone (15) or fewer peaks of growth hormone between 2:00 and 6:00 A.M. (14) have been observed. In nondiabetic subjects, the physiological nocturnal increase in growth hormone does not seem to influence carbohydrate metabolism the next morning (23). By contrast, administration of pulsed growth hormone to type 1 diabetic subjects has a marked effect on hepatic glucose output, and even moderate elevations in growth hormone can lead to poor metabolic control within 8 -10 h (24).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Evening Alcohol Consumption on Next-Morning Glucose Control in Type 1 Diabetes

et al. 2001

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OBJECTIVE—Alcohol is associated with acute hypoglycemia in patients with type 1 diabetes. After drinking alcohol in the evening, delayed hypoglycemia has also been described, although its cause is unknown. We performed a controlled study to investigate this phenomenon. RESEARCH DESIGN AND METHODS—We admitted six men with type 1 diabetes (aged 19–51 years, HbA1c 7.0–10.3%) on two occasions, from 5:00 p.m. to 12:00 noon the following day. They received regular insulin injections before standardized meals, at 6:00 p.m. and 8:00 a.m., and a basal insulin infusion (0.15 mU · kg−1 · min−1) from 11:00 p.m. They drank either dry white wine (0.75 g/kg alcohol) or mineral water at 9:00 p.m. over 90 min. Blood glucose, alcohol, insulin, cortisol, growth hormone, and glucagon levels were measured. RESULTS—Blood ethanol reached a mean (SEM) peak of 19.1 (1.2) mmol/l and was undetectable by 8:00 a.m. There were no significant differences in evening or overnight blood glucose levels between the studies. In the morning, fasting and postprandial blood glucose levels were significantly lower after consumption of wine (postprandial peak 8.9 [1.7] vs. 15 [1.5] mmol/l, P < 0.01), and from 10:00 a.m., five subjects required treatment for hypoglycemia (nadir 1.9–2.9 mmol/l). None of the subjects had hypoglycemia after consumption of water. After consumption of wine, growth hormone secretion was significantly reduced between midnight and 4:00 a.m. (area under the curve 2.1 [1.1] vs. 6.5 [2.1] μg · l–1 · h–1, P = 0.04). There were no differences in insulin or other hormone levels. CONCLUSIONS—In type 1 diabetes, moderate consumption of alcohol in the evening may predispose patients to hypoglycemia after breakfast the next morning. This is associated with reduced nocturnal growth hormone secretion. Patients should be informed of this risk and advised regarding appropriate preventative measures.

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“…Endogenous hormone secretion was inhibited by continuous infusion of somatostatin (S; 0.11 µU kg -1 min -1 ; −5-360 min; UCB Pharma, Vienna, Austria). In addition, insulin (0.065 mU kg -1 min -1 ; Actrapid, Novo Nordisk, Bagsvaerd, Denmark), glucagon (0.9 ng kg -1 min -1 ; Novo Nordisk, Vienna, Austria) and growth hormone (2.0 ng kg -1 min -1 ; Genotropin, Upjohn and Pharmacia, Vienna, Austria) [24] were replaced from 0 to 360 min to provide for their fasting peripheral concentrations. A balanced AA mixture (0.2 g kg -1 h -1 ; Aminoplasmal 10% without electrolytes, Braun, Melsungen, Germany) was infused (0-360 min) in order to create postprandial conditions of increased plasma AA concentrations as described previously [10].…”

Section: Methodsmentioning

confidence: 99%

Direct and indirect effects of amino acids on hepatic glucose metabolism in humans

et al. 2003

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Aim/hypothesis. The study was designed to examine the contribution of direct (substrate-mediated) and indirect (hormone-mediated) effects of amino acids on hepatic glucose metabolism in healthy men. Methods. The protocols were: (i) CON+S (n=7): control conditions with somatostatin to inhibit endogenous hormone release resulting in fasting plasma concentrations of amino acids, insulin (~28 pmol/l) and glucagon (~65 ng/l), (ii) AA+S (n=7): amino acid infusion-fasting insulinaemia-fasting glucagonaemia, (iii) GLUC+S (n=6): fasting amino acids-fasting insulinaemia-hyperglucagonaemia (~99 ng/l) and (iv) AA-S (n=5): amino acid infusion without somatostatin resulting in amino acid-induced hyperinsulinaemia (~61 pmol/l)-hyperglucagonaemia (~147 ng/l). Net glycogenolysis was calculated from liver glycogen concentrations using 13 C nuclear magnetic resonance spectroscopy. Total gluconeogenesis (GNG) was calculated by subtracting net glycogenolysis from endogenous glucose production (EGP) which was measured with [6,6-2 H 2 ]glucose. Net GNG was assessed with the 2 H 2 O method. Results. During AA+S and GLUC+S, plasma glucose increased by about 50% (p<0.01) due to a comparable rise in EGP. This was associated with a 53-% (p<0.05) and a 65% increase (p<0.01) of total and net GNG during AA+S, whereas net glycogenolysis rose by 70% (p<0.001) during GLUC+S. During AA-S, plasma glucose remained unchanged despite nearlydoubled (p<0.01) total GNG. Conclusion/interpretation. Conditions of postprandial amino acid elevation stimulate secretion of insulin and glucagon without affecting glycaemia despite markedly increased gluconeogenesis. Impaired insulin secretion unmasks the direct gluconeogenic effect of amino acids and increases plasma glucose. [Diabetologia (2003) 46:917-925]

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Failure of nocturnal changes in growth hormone to alter carbohydrate tolerance the following morning

Cited by 10 publications

References 47 publications

Effect of Growth Hormone (GH) on Glycerol and Free Fatty Acid Metabolism during Exhaustive Exercise in GH-Deficient Adults

Effect of Growth Hormone (GH) on Glycerol and Free Fatty Acid Metabolism during Exhaustive Exercise in GH-Deficient Adults

The Effect of Evening Alcohol Consumption on Next-Morning Glucose Control in Type 1 Diabetes

Direct and indirect effects of amino acids on hepatic glucose metabolism in humans

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