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Growth hormone, insulin-like growth factor-1 and insulin resistance in cirrhosis.
Hepatology. 1994 Feb; 19(2):322-8.Hep

Abstract

Cirrhosis is characterized by paradoxical growth hormone secretion in response to glucose and insulin infusion. To ascertain whether this abnormality contributes to insulin resistance, euglycemic hyperinsulinemic glucose clamps were performed on six patients with cirrhosis and six normal control subjects. Each patient with cirrhosis underwent two clamps in random order, a clamp with somatostatin (250 micrograms/hr) together with insulin and glucagon replacement, and a control clamp without somatostatin. The normal subjects underwent the control clamp only. During the control clamp, growth hormone levels were considerably higher in the patients with cirrhosis (6.1 +/- 0.4 vs. 0.5 +/- 0.4 mU/L, p < 0.02), and glucose uptake was considerably lower (3.29 +/- 0.56 vs. 9.52 +/- 1.14 mg/kg/min, p < 0.001). Indirect calorimetry indicated that the defect was accounted for by lower nonoxidative glucose disposal (1.23 +/- 0.45 vs. 6.00 +/- 0.73, p < 0.001). Peripheral glucose uptake, exemplified by forearm glucose uptake (0.27 +/- 0.04 vs. 1.22 +/- 0.42 mg/100 ml/min, p < 0.02), and calculated insulin sensitivity (24 +/- 8 vs. 114 +/- 20 microliters/kg/min per mU/L) were particularly diminished. In the patients with cirrhosis somatostatin suppressed growth hormone levels (6.1 +/- 1.2 to 1.2 +/- 0.4 mU/L, p < 0.05). However, no significant changes occurred in whole-body glucose uptake (3.29 +/- 0.56 vs 3.01 +/- 0.54 mg/kg/min), forearm glucose uptake (0.27 +/- 0.04 vs 0.30 +/- 0.01 mg/100 ml/min) or insulin sensitivity (24 +/- 8 vs, 35 +/- 10 microliters/kg/min/mU/L, p = 0.42).(

ABSTRACT

TRUNCATED AT 250 WORDS)

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Authors+Show Affiliations

Shmueli E
Gastroenterology and Liver Unit, Royal Victoria Infirmary, Newcastle Upon Tyne, United Kingdom.
Stewart M
No affiliation info available
Alberti KG
No affiliation info available
Record CO
No affiliation info available

MeSH

AdultC-PeptideCalorimetry, IndirectFatty Acids, NonesterifiedGlucoseGlucose Clamp TechniqueGrowth HormoneHumansInsulin ResistanceInsulin-Like Growth Factor ILiverLiver Cirrhosis, AlcoholicMaleMiddle AgedSomatostatin

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

7904978

Citation

Shmueli, E, et al. "Growth Hormone, Insulin-like Growth Factor-1 and Insulin Resistance in Cirrhosis." Hepatology (Baltimore, Md.), vol. 19, no. 2, 1994, pp. 322-8.
Shmueli E, Stewart M, Alberti KG, et al. Growth hormone, insulin-like growth factor-1 and insulin resistance in cirrhosis. Hepatology. 1994;19(2):322-8.
Shmueli, E., Stewart, M., Alberti, K. G., & Record, C. O. (1994). Growth hormone, insulin-like growth factor-1 and insulin resistance in cirrhosis. Hepatology (Baltimore, Md.), 19(2), 322-8.
Shmueli E, et al. Growth Hormone, Insulin-like Growth Factor-1 and Insulin Resistance in Cirrhosis. Hepatology. 1994;19(2):322-8. PubMed PMID: 7904978.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Growth hormone, insulin-like growth factor-1 and insulin resistance in cirrhosis. AU - Shmueli,E, AU - Stewart,M, AU - Alberti,K G, AU - Record,C O, PY - 1994/2/1/pubmed PY - 1994/2/1/medline PY - 1994/2/1/entrez SP - 322 EP - 8 JF - Hepatology (Baltimore, Md.) JO - Hepatology VL - 19 IS - 2 N2 - Cirrhosis is characterized by paradoxical growth hormone secretion in response to glucose and insulin infusion. To ascertain whether this abnormality contributes to insulin resistance, euglycemic hyperinsulinemic glucose clamps were performed on six patients with cirrhosis and six normal control subjects. Each patient with cirrhosis underwent two clamps in random order, a clamp with somatostatin (250 micrograms/hr) together with insulin and glucagon replacement, and a control clamp without somatostatin. The normal subjects underwent the control clamp only. During the control clamp, growth hormone levels were considerably higher in the patients with cirrhosis (6.1 +/- 0.4 vs. 0.5 +/- 0.4 mU/L, p < 0.02), and glucose uptake was considerably lower (3.29 +/- 0.56 vs. 9.52 +/- 1.14 mg/kg/min, p < 0.001). Indirect calorimetry indicated that the defect was accounted for by lower nonoxidative glucose disposal (1.23 +/- 0.45 vs. 6.00 +/- 0.73, p < 0.001). Peripheral glucose uptake, exemplified by forearm glucose uptake (0.27 +/- 0.04 vs. 1.22 +/- 0.42 mg/100 ml/min, p < 0.02), and calculated insulin sensitivity (24 +/- 8 vs. 114 +/- 20 microliters/kg/min per mU/L) were particularly diminished. In the patients with cirrhosis somatostatin suppressed growth hormone levels (6.1 +/- 1.2 to 1.2 +/- 0.4 mU/L, p < 0.05). However, no significant changes occurred in whole-body glucose uptake (3.29 +/- 0.56 vs 3.01 +/- 0.54 mg/kg/min), forearm glucose uptake (0.27 +/- 0.04 vs 0.30 +/- 0.01 mg/100 ml/min) or insulin sensitivity (24 +/- 8 vs, 35 +/- 10 microliters/kg/min/mU/L, p = 0.42).(ABSTRACT TRUNCATED AT 250 WORDS) SN - 0270-9139 UR - https://www.unboundmedicine.com/medline/citation/7904978/Growth_hormone_insulin_like_growth_factor_1_and_insulin_resistance_in_cirrhosis_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&amp;sid=nlm:pubmed&amp;issn=0270-9139&amp;date=1994&amp;volume=19&amp;issue=2&amp;spage=322 DB - PRIME DP - Unbound Medicine ER -