Role of hyperglucagonemia in catabolism associated with type 1 diabetes: effects on leucine metabolism and the resting metabolic rate

Role of hyperglucagonemia in catabolism associated with type 1 diabetes: effects on leucine metabolism and the resting metabolic rate. M R Charlton and K S Nair Endocrine Research Unit, the Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA. Abstract The catabolic state of poorly controlled...

Celý popis

Uloženo v:
Podrobná bibliografie
Vydáno v:Diabetes (New York, N.Y.) Ročník 47; číslo 11; s. 1748 - 1756
Hlavní autoři: Charlton, M R, Nair, K S
Médium: Journal Article
Jazyk:angličtina
Vydáno: Alexandria, VA American Diabetes Association 01.11.1998
Témata:
Adult
Amino acid metabolism
Amino Acids - blood
Basal Metabolism
Biological and medical sciences
Calorimetry, Indirect
Diabetes Mellitus, Type 1 - blood
Diabetes Mellitus, Type 1 - drug therapy
Diabetes Mellitus, Type 1 - metabolism
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Energy Metabolism
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Female
Glucagon
Glucagon - blood
Humans
Insulin - administration & dosage
Insulin - blood
Insulin - therapeutic use
Kinetics
Leucine
Leucine - blood
Male
Medical sciences
Oxidation-Reduction
Physiological aspects
Proteins - metabolism
Regression Analysis
Somatostatin
Type 1 diabetes
Endocrinopathy
Human
Immunopathology
Pancreatic hormone
Glucagon
Pathophysiology
Insulin dependent diabetes
Autoimmune disease
Catabolism
Basal metabolism
Hyperglucagonemia
ISSN:0012-1797, 1939-327X
On-line přístup:Získat plný text
Tagy: Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
Popis
Shrnutí:Role of hyperglucagonemia in catabolism associated with type 1 diabetes: effects on leucine metabolism and the resting metabolic rate. M R Charlton and K S Nair Endocrine Research Unit, the Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA. Abstract The catabolic state of poorly controlled type 1 diabetes has largely been attributed to insulin deficiency. However, the role of hyperglucagonemia, which occurs concomitantly with insulin deficiency, has not been fully investigated. We studied the effects of hyperglucagonemia during insulin deprivation on energy expenditure (using indirect calorimetry) and protein metabolism (using L-[1-(13)C,15N]leucine and L-[1-(13)C]leucine as tracers) in 12 type 1 diabetic subjects. Five protocols were used: insulin treatment, insulin deprivation, insulin deprivation with suppression of endogenous glucagon with somatostatin (SRIH) and growth hormone replacement, insulin deprivation with endogenous glucagon suppression with SRIH (no growth hormone replacement), and insulin deprivation with SRIH and a high level of glucagon replacement (no growth hormone replacement). It was observed that leucine oxidation and the resting metabolic rate (RMR) were significantly lower during insulin treatment and insulin deprivation with concomitant SRIH infusion (lowering glucagon) than during insulin deprivation alone. Replacement of glucagon at a high level during SRIH infusion in the insulin-deprived state increased leucine oxidation and the RMR. Hyperglucagonemia was also associated with a trend for decreased protein synthesis. Hyperglucagonemia did not affect leucine transamination. Insulin replacement decreased leucine flux and oxidation. Leucine oxidation (R2 = 0.79) and the RMR (R2 = 0.81) were seen, by multiple regression analysis, to correlate with glucagon levels and not with other hormones. We conclude that while insulin deficiency increases protein breakdown, hyperglucagonemia is primarily responsible for the increased leucine oxidation and RMR seen during insulin deprivation.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
content type line 14
ObjectType-Feature-2
content type line 23
ISSN:0012-1797
1939-327X
DOI:10.2337/diabetes.47.11.1748