Growth Hormone Therapy with Diet Restriction in Obese Patients with Type 2 Diabetes Mellitus.
- Author:
Su Youn NAM
1
;
Kyung Rae KIM
;
Young Duk SONG
;
Sung Kil LIM
;
Hyun Chul LEE
;
Kap Bum HUH
Author Information
1. Division of endocrinology, Department of Internal Medicine, Yonsei University Medical College, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Type 2 DM;
Obesity;
Insulin resistance;
Growth hormone
- MeSH:
Adipose Tissue;
Anabolic Agents;
Blood Glucose;
Body Composition;
Body Weight;
Cholesterol;
Diabetes Mellitus, Type 2*;
Diet*;
Dyslipidemias;
Glucose;
Glucose Tolerance Test;
Growth Hormone*;
Humans;
Insulin Resistance;
Intra-Abdominal Fat;
Levodopa;
Lipid Metabolism;
Lipolysis;
Metabolism;
Muscle, Skeletal;
Obesity;
Risk Factors;
Subcutaneous Fat;
Triglycerides;
Umbilicus
- From:Journal of Korean Society of Endocrinology
1999;14(1):27-39
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Insulin resistance in obesity constitutes an independent risk factor for the development of type 2 diabetes mellitus (DM). Insulin resistance in obese DM can be improved by a decrease in visceral fat and an increase in skeletal muscle which may influence insulin sensitivity via its capacity to uptake glucose load. Diet restriction as a treatment for obesity causes protein catabolism which results in a decrease in muscle mass. Growth hormone (GH) therapy accelerates a lipolysis and promotes protein conservation. We evaluated the effects of GH therapy with diet restriction on lipolysis and anabolism, which can change body composition, insulin resistance and lipid metabolism in obese DM. METHODS: Eighteen newly-diagnosed obese type 2 DM patients (42-56 yrs) were treated with recombinant human GH (GH; 0.06 unit/kg ideal body weight#/day, 3 times/wk) and with diet restriction (25 kcal/kg ideal body weight/day) for 12 weeks. They underwent anthropometric measurement, bioelectrical impedence for total body fat and lean body mass, as well as computed tomography for visceral and subcutaneous fat at the umbilicus level and the muscle area at the mid-thigh level. All subjects underwent a standard oral glucose tolerance test (OGTT) and GH response to L-dopa stimulation. The glucose disposal rate was measured during an euglycemic hyperinsulinemic clamp study. RESULTS: 1. The fraction of body weight lost as fat was significantly greater and the visceral fat area was decreased more in the GH-treated group than in the control group. There was a significant loss of lean body mass and muscle area in the control group, whereas there was an increase in lean body mass and muscle area in GH-treated group. 2. The glucose disposal rate was significantly increased only in the GH-treated group and it was negatively correlated with the ratio of the visceral fat area/muscle area. The serum glucose levels, insulin-area under the curve (AUC) and free fatty acid (FFA)-AUC during OGTT and HbAlc were significantly decreased after GH treatment. The decrease in FFA-AUC was positively correlated with the decrease in the visceral fat area. 3. Total cholesterol and triglyceride were decreased in both groups. LDL-cholesterol was decreased in only the GH-treated group. 4. The GH response to L-dopa stimulatian was blunted in aU subjects and after treatment, the GH response was increased. The insulin-like growth factor-I level was inereased 1.6-fold after the GH treatment. CONCLUSION: This study suggested that in obese DM fed a hypocaloric diet, GH treatment exerted a decrease in visceral fat and an increase in muscle mass via accelerated lipolytic and anabolic effects which could result in the improvement of insulin resistance, glucose metabolism and dyslipidemia.
