Glucose, fat, and protein kinetics in patients with primary and secondary hyperparathyroidism.
We performed a series of isotopic studies in 16 normal volunteers, four patients with secondary hyperparathyroidism (SHPT), and in nine patients with primary hyperparathyroidism (PHPT). Using the primed constant infusion of stable and radioisotopes, we have determined glucose, glycerol, free fatty acids, and urea kinetics, as well as glucose oxidation. Measurements were performed both in the basal state and during glucose infusion (4 mg/kg body weight/min). Compared with normal volunteers, PHPT patients are intolerant of glucose because of a limited suppression of endogenous glucose turnover during glucose infusion (34% versus 96% suppression). In addition, the plasma cortisol level increased in the PHPT patients during glucose infusion. Glucose oxidation and fat kinetics in both PHPT patients and volunteers were similar, but the rate of net protein loss was significantly greater in the PHPT patients than in the volunteers (2.1 +/- 0.5 versus 1.4 +/- 0.2 gm/kg/day). Rates of VO2 in the PHPT patients and volunteers were similar, but the value in the SHPT patients was higher (120 +/- 9 versus 142 +/- 20 mumol/kg/min for PHPT and SHPT patients, respectively). The SHPT patients had significantly increased rates of glucose turnover, glucose clearance, and glycerol turnover, compared with the other two groups, as well as an increased reliance on glucose for energy. We conclude from these studies that (1) SHPT patients are catabolic and have increased rates of glucose and fat turnover; (2) PHPT patients have limited suppression of endogenous glucose turnover after glucose infusion compared with volunteers and higher rates of net protein loss; (3) fat metabolism and glucose utilization are unimpaired in PHPT patients; and (4) these alterations in metabolism and hormonal response to glucose infusion suggest that some of the symptoms seen in these patients may have a metabolic-hormonal basis.
Shaw
J H
JH
Department of Surgery, Auckland Hospital, New Zealand.
Croxon
M
M
Holdaway
I
I
Collins
J P
JP
Wolfe
R R
RR
D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D005227:Fatty Acids / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000008:administration & dosage / Q000378:metabolism*; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006961:Hyperparathyroidism / Q000097:blood / Q000378:metabolism*; D006962:Hyperparathyroidism, Secondary / Q000097:blood / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption; D011506:Proteins / Q000378:metabolism*; D014508:Urea / Q000378:metabolism
D001786:Blood Glucose; D005227:Fatty Acids; D007328:Insulin; D011506:Proteins; D014508:Urea; D005947:Glucose; D005990:Glycerol; D006854:Hydrocortisone