DECREASED HEPATIC GLUCAGON-RESPONSES IN TYPE-1 (INSULIN-DEPENDENT) DIABETES-MELLITUS

被引:28
作者
ORSKOV, L
ALBERTI, KGMM
MENGEL, A
MOLLER, N
PEDERSEN, O
RASMUSSEN, O
SEEFELDT, T
SCHMITZ, O
机构
[1] AARHUS UNIV,INST EXPTL CLIN RES,DK-8000 AARHUS,DENMARK
[2] RANDERS CENT HOSP,DEPT MED,RANDERS,DENMARK
[3] HVIDOVRE UNIV HOSP,KLAMPENBORG,DENMARK
[4] UNIV NEWCASTLE UPON TYNE,DEPT MED,NEWCASTLE TYNE NE1 7RU,TYNE & WEAR,ENGLAND
关键词
TYPE-1; DIABETES-MELLITUS; GLUCAGON; HEPATIC GLUCOSE PRODUCTION; GLUCOSE COUNTERREGULATION; GROWTH-HORMONE; SUBCUTANEOUS INSULIN; INDUCED HYPOGLYCEMIA; AUTO-REGULATION; PLASMA-GLUCOSE; BLOOD-GLUCOSE; RESISTANCE; HUMANS; EPINEPHRINE;
D O I
10.1007/BF00403290
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The effect of glucagon infusion on hepatic glucose production during euglycaemia was evaluated in seven Type 1 (insulin-dependent) diabetic patients and in ten control subjects. In the diabetic subjects normoglycaemia was maintained during the night preceding the study by a variable intravenous insulin and glucose infusion. During the study endogenous insulin secretion was suppressed by somatostain (450-mu-g/h) and replaced by insulin infusion (0.15 mU.kg-1.min-1). H-3-glucose was infused for isotopic determination of glucose turnover. Plasma glucose was clamped at 5 mmol/l for 2 h 30 min and glucagon (1.5 ng.kg-1.min-1) was then infused for the following 3 h. Hepatic glucose production and glucose utilisation were measured during the first, second and third hour of the glucagon infusion. Basal hepatic glucose production (just prior to glucagon infusion) was similar in diabetic (1.2 +/- 0.3 mg.kg-1.min-1) and control (1.6 +/- 0.1 mg.kg-1.min-1) subjects. In diabetic patients hepatic glucose production rose slowly to 2.1 +/- 0.5 mg.kg-1.min-1 during the first hours of glucagon infusion and stabilized at this level (2.4 +/- 0.5 mg.kg-1.min-1) in the third hour. In control subjects hepatic glucose production increased sharply to higher levels than in the diabetic subjects (3.4 +/- 0.3 mg.kg-1.min-1) during the first and second hour of glucagon infusion (p < 0.05) and then gradually fell (2.9 +/- 0.4 mg.kg-1.min-1) during the third hour. In conclusion, when stimulated with glucagon at a physiologic plasma concentration diabetic patients had 1) an overall reduced hepatic glucose production response and 2) an abnormal sluggish response pattern. These abnormalities may imply inappropriate counter-regulation following a hypoglycaemic episode.
引用
收藏
页码:521 / 526
页数:6
相关论文
共 40 条
  • [11] THE PANCREATIC-ADRENOCORTICAL-PITUITARY CLAMP TECHNIQUE FOR STUDY OF COUNTERREGULATION IN HUMANS
    DEFEO, P
    PERRIELLO, G
    VENTURA, MM
    BRUNETTI, P
    SANTEUSANIO, F
    GERICH, JE
    BOLLI, GB
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1987, 252 (04): : E565 - E570
  • [12] DEMONSTRATION OF A ROLE FOR GROWTH-HORMONE IN GLUCOSE COUNTERREGULATION
    DEFEO, P
    PERRIELLO, G
    TORLONE, E
    VENTURA, MM
    SANTEUSANIO, F
    BRUNETTI, P
    GERICH, JE
    BOLLI, GB
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 256 (06): : E835 - E843
  • [13] CONTRIBUTION OF CORTISOL TO GLUCOSE COUNTERREGULATION IN HUMANS
    DEFEO, P
    PERRIELLO, G
    TORLONE, E
    VENTURA, MM
    FANELLI, C
    SANTEUSANIO, F
    BRUNETTI, P
    GERICH, JE
    BOLLI, GB
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (01): : E35 - E42
  • [14] DEFRONZO RA, 1982, DIABETOLOGIA, V23, P313
  • [15] HORMONAL MECHANISMS OF RECOVERY FROM INSULIN-INDUCED HYPOGLYCEMIA IN MAN
    GERICH, J
    DAVIS, J
    LORENZI, M
    RIZZA, R
    BOHANNON, N
    KARAM, J
    LEWIS, S
    KAPLAN, R
    SCHULTZ, T
    CRYER, P
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1979, 236 (04): : E380 - E385
  • [16] Gerich J., 1980, METABOLISM, V29, P1164
  • [17] GLUCOSE COUNTERREGULATION AND ITS IMPACT ON DIABETES-MELLITUS
    GERICH, JE
    [J]. DIABETES, 1988, 37 (12) : 1608 - 1617
  • [18] GERICH JE, 1976, J CLIN INVEST, V57, P877
  • [19] THE ROLE OF AUTOREGULATION OF THE HEPATIC GLUCOSE-PRODUCTION IN MAN - RESPONSE TO A PHYSIOLOGICAL DECREMENT IN PLASMA-GLUCOSE
    HANSEN, I
    FIRTH, R
    HAYMOND, M
    CRYER, P
    RIZZA, R
    [J]. DIABETES, 1986, 35 (02) : 186 - 191
  • [20] HARRISON J, 1988, J CLIN CHEM CLIN BIO, V26, P141