Progesterone administration induced impairment of insulin suppression of hepatic glucose production

T. Nelson, G. Shulman, D. Grainger, Michael Peter Diamond

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Objective: To assess whether P administration impairs insulin-mediated glucose uptake. Design: Two-step euglycemic hyperinsulinemic clamp studies. Setting: Rats studied with (n = 11) or without (n = 10) P treatment. Participants: Conscious, unstressed, oophorectomized female rats. Main Outcome Measures: Plasma glucose and insulin levels and the rates of glucose turnover results. Results: Fasting glucose (115 ± 5 versus 109 ± 4 mg/dL; conversion factor to SI units 0.05551) and insulin (1.67 ± 0.24 versus 1.51 ± 0.22 ng/mL; conversion factor to SI units 174.5) levels were not significantly different in the control and P treated groups, respectively. However, the basal rate of glucose turnover was significantly higher in P- treated rats (8.38 ± 0.50 versus 6.59 ± 0.35 mg/kg per minute in controls. During low-dose insulin infusion (2 mU/kg per minute), there was no difference in glucose or insulin levels, or the rate of glucose utilization; however, residual hepatic glucose production was significantly greater in the P group (5.34 ± 0.68 versus 2.57 ± 1.00 mg/kg per minute) in controls. At high-dose insulin infusion (10 mU/kg per minute), hepatic glucose production was completely suppressed in both groups; there was no difference in insulin sensitivity as assessed by the glucose utilization rate or the ratio of glucose uptake to insulin level. Conclusions: Chronic P therapy does not alter insulin-mediated glucose utilization in peripheral tissues but does reduce the ability of insulin to suppress endogenous hepatic glucose production.

Original languageEnglish (US)
Pages (from-to)491-496
Number of pages6
JournalFertility and Sterility
Volume62
Issue number3
DOIs
StatePublished - Jan 1 1994
Externally publishedYes

Fingerprint

Progesterone
Insulin
Glucose
Liver
International System of Units
Aptitude
Glucose Clamp Technique
Insulin Resistance
Fasting
Outcome Assessment (Health Care)

Keywords

  • glucose production
  • glucose utilization
  • insulin
  • Progesterone

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology

Cite this

Progesterone administration induced impairment of insulin suppression of hepatic glucose production. / Nelson, T.; Shulman, G.; Grainger, D.; Diamond, Michael Peter.

In: Fertility and Sterility, Vol. 62, No. 3, 01.01.1994, p. 491-496.

Research output: Contribution to journalArticle

@article{8dc0541458ec4d608f040c8f043d8073,
title = "Progesterone administration induced impairment of insulin suppression of hepatic glucose production",
abstract = "Objective: To assess whether P administration impairs insulin-mediated glucose uptake. Design: Two-step euglycemic hyperinsulinemic clamp studies. Setting: Rats studied with (n = 11) or without (n = 10) P treatment. Participants: Conscious, unstressed, oophorectomized female rats. Main Outcome Measures: Plasma glucose and insulin levels and the rates of glucose turnover results. Results: Fasting glucose (115 ± 5 versus 109 ± 4 mg/dL; conversion factor to SI units 0.05551) and insulin (1.67 ± 0.24 versus 1.51 ± 0.22 ng/mL; conversion factor to SI units 174.5) levels were not significantly different in the control and P treated groups, respectively. However, the basal rate of glucose turnover was significantly higher in P- treated rats (8.38 ± 0.50 versus 6.59 ± 0.35 mg/kg per minute in controls. During low-dose insulin infusion (2 mU/kg per minute), there was no difference in glucose or insulin levels, or the rate of glucose utilization; however, residual hepatic glucose production was significantly greater in the P group (5.34 ± 0.68 versus 2.57 ± 1.00 mg/kg per minute) in controls. At high-dose insulin infusion (10 mU/kg per minute), hepatic glucose production was completely suppressed in both groups; there was no difference in insulin sensitivity as assessed by the glucose utilization rate or the ratio of glucose uptake to insulin level. Conclusions: Chronic P therapy does not alter insulin-mediated glucose utilization in peripheral tissues but does reduce the ability of insulin to suppress endogenous hepatic glucose production.",
keywords = "glucose production, glucose utilization, insulin, Progesterone",
author = "T. Nelson and G. Shulman and D. Grainger and Diamond, {Michael Peter}",
year = "1994",
month = "1",
day = "1",
doi = "10.1016/S0015-0282(16)56936-2",
language = "English (US)",
volume = "62",
pages = "491--496",
journal = "Fertility and Sterility",
issn = "0015-0282",
publisher = "Elsevier Inc.",
number = "3",

}

TY - JOUR

T1 - Progesterone administration induced impairment of insulin suppression of hepatic glucose production

AU - Nelson, T.

AU - Shulman, G.

AU - Grainger, D.

AU - Diamond, Michael Peter

PY - 1994/1/1

Y1 - 1994/1/1

N2 - Objective: To assess whether P administration impairs insulin-mediated glucose uptake. Design: Two-step euglycemic hyperinsulinemic clamp studies. Setting: Rats studied with (n = 11) or without (n = 10) P treatment. Participants: Conscious, unstressed, oophorectomized female rats. Main Outcome Measures: Plasma glucose and insulin levels and the rates of glucose turnover results. Results: Fasting glucose (115 ± 5 versus 109 ± 4 mg/dL; conversion factor to SI units 0.05551) and insulin (1.67 ± 0.24 versus 1.51 ± 0.22 ng/mL; conversion factor to SI units 174.5) levels were not significantly different in the control and P treated groups, respectively. However, the basal rate of glucose turnover was significantly higher in P- treated rats (8.38 ± 0.50 versus 6.59 ± 0.35 mg/kg per minute in controls. During low-dose insulin infusion (2 mU/kg per minute), there was no difference in glucose or insulin levels, or the rate of glucose utilization; however, residual hepatic glucose production was significantly greater in the P group (5.34 ± 0.68 versus 2.57 ± 1.00 mg/kg per minute) in controls. At high-dose insulin infusion (10 mU/kg per minute), hepatic glucose production was completely suppressed in both groups; there was no difference in insulin sensitivity as assessed by the glucose utilization rate or the ratio of glucose uptake to insulin level. Conclusions: Chronic P therapy does not alter insulin-mediated glucose utilization in peripheral tissues but does reduce the ability of insulin to suppress endogenous hepatic glucose production.

AB - Objective: To assess whether P administration impairs insulin-mediated glucose uptake. Design: Two-step euglycemic hyperinsulinemic clamp studies. Setting: Rats studied with (n = 11) or without (n = 10) P treatment. Participants: Conscious, unstressed, oophorectomized female rats. Main Outcome Measures: Plasma glucose and insulin levels and the rates of glucose turnover results. Results: Fasting glucose (115 ± 5 versus 109 ± 4 mg/dL; conversion factor to SI units 0.05551) and insulin (1.67 ± 0.24 versus 1.51 ± 0.22 ng/mL; conversion factor to SI units 174.5) levels were not significantly different in the control and P treated groups, respectively. However, the basal rate of glucose turnover was significantly higher in P- treated rats (8.38 ± 0.50 versus 6.59 ± 0.35 mg/kg per minute in controls. During low-dose insulin infusion (2 mU/kg per minute), there was no difference in glucose or insulin levels, or the rate of glucose utilization; however, residual hepatic glucose production was significantly greater in the P group (5.34 ± 0.68 versus 2.57 ± 1.00 mg/kg per minute) in controls. At high-dose insulin infusion (10 mU/kg per minute), hepatic glucose production was completely suppressed in both groups; there was no difference in insulin sensitivity as assessed by the glucose utilization rate or the ratio of glucose uptake to insulin level. Conclusions: Chronic P therapy does not alter insulin-mediated glucose utilization in peripheral tissues but does reduce the ability of insulin to suppress endogenous hepatic glucose production.

KW - glucose production

KW - glucose utilization

KW - insulin

KW - Progesterone

UR - http://www.scopus.com/inward/record.url?scp=0028133093&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028133093&partnerID=8YFLogxK

U2 - 10.1016/S0015-0282(16)56936-2

DO - 10.1016/S0015-0282(16)56936-2

M3 - Article

VL - 62

SP - 491

EP - 496

JO - Fertility and Sterility

JF - Fertility and Sterility

SN - 0015-0282

IS - 3

ER -