Effect of testosterone replacement on whole body glucose utilisation and other cardiovascular risk factors in males with idiopathic hypogonadotrophic hypogonadism

Devjit Tripathy, P. Shah, R. Lakshmy, K. S. Reddy

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

Background: Excessive testosterone in males or estrogens in females could explain their differences in coronary heart disease event rates. As a contraceptive testosterone is likely to be used at large scale the role of testosterone in increasing the risks of coronary heart disease needs investigation. Aim: To look at the role of testosterone in development of insulin resistance and other cardiovascular risk factors. Design: Prospective, before-after study on ten male subjects with idiopathic hypogonadotrophic hypogonadism pre- and post-testosterone replacement therapy; outcome measure; anthropometry, lipoprotein profile and M value (whole body glucose disposal rates on standard hyperinsulinemic euglycemic clamp; at insulin infusion rate: 40 mU · m-2). Results: Pre-treatment serum testosterone was 0.43 (0.515) ng · ml-1 LH was 1.29 (0.08) IU · L- 1, and FSH was 1.54 (0.08) IU · L-1. None had glucose intolerance. After replacement testosterone levels increased to 9.4 ng · mL-1 (p = 0.005); weight increase of 5.0 kg (p=0.140), body mass index increase of 1.2 kg · m-2 (p=0.28) and the change in waist to hip ratio (p=0.31) were not statistically significant. M-value (mg. kg · min-1) did not change after testosterone therapy (5.86 [0.72] vs 5.29 [0.82], p=0.62). Insulin levels (mU · L-1) achieved during the clamps were 89.5 (14.2) before and 146 (32.2) after androgen therapy (p=0.127). There was no change in glucose area under curve (mg · min · dL-1) (14406 [502.2] vs 12557 [826.5], p=0.312). On testosterone replacement therapy total and LDL cholesterol levels (mg · dL- 1) declined (122.5 [13.4] vs 91.6 [5.0], p=0.04; 65.9 [9.9] vs 39.4 [7.3], p=0.05); Ratio of total cholesterol to HDL ratio also decreased significantly (p=0.05). Changes of serum triglycerides (p=0.25) and HDL cholesterol (p=0.19) did not attain statistical significance. Conclusions: Insulin sensitivity does not decrease on testosterone replacement therapy of male subjects with idiopathic hypogonadotrophic hypogonadism. Testosterone replacement was associated with decrease in other cardiovascular risk factors.

Original languageEnglish (US)
Pages (from-to)642-645
Number of pages4
JournalHormone and Metabolic Research
Volume30
Issue number10
StatePublished - 1998
Externally publishedYes

Fingerprint

Testosterone
Glucose
Insulin
Clamping devices
HDL Cholesterol
Coronary Disease
Insulin Resistance
Idiopathic Hypogonadotropic Hypogonadism
Anthropometry
Therapeutics
Glucose Clamp Technique
Glucose Intolerance
Waist-Hip Ratio
Contraceptive Agents
Serum
LDL Cholesterol
Androgens
Lipoproteins
Area Under Curve
Estrogens

Keywords

  • Androgens
  • Cardiovascular Risk Factor
  • Hypogonadism
  • Insulin Resistance
  • Male

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

Effect of testosterone replacement on whole body glucose utilisation and other cardiovascular risk factors in males with idiopathic hypogonadotrophic hypogonadism. / Tripathy, Devjit; Shah, P.; Lakshmy, R.; Reddy, K. S.

In: Hormone and Metabolic Research, Vol. 30, No. 10, 1998, p. 642-645.

Research output: Contribution to journalArticle

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abstract = "Background: Excessive testosterone in males or estrogens in females could explain their differences in coronary heart disease event rates. As a contraceptive testosterone is likely to be used at large scale the role of testosterone in increasing the risks of coronary heart disease needs investigation. Aim: To look at the role of testosterone in development of insulin resistance and other cardiovascular risk factors. Design: Prospective, before-after study on ten male subjects with idiopathic hypogonadotrophic hypogonadism pre- and post-testosterone replacement therapy; outcome measure; anthropometry, lipoprotein profile and M value (whole body glucose disposal rates on standard hyperinsulinemic euglycemic clamp; at insulin infusion rate: 40 mU · m-2). Results: Pre-treatment serum testosterone was 0.43 (0.515) ng · ml-1 LH was 1.29 (0.08) IU · L- 1, and FSH was 1.54 (0.08) IU · L-1. None had glucose intolerance. After replacement testosterone levels increased to 9.4 ng · mL-1 (p = 0.005); weight increase of 5.0 kg (p=0.140), body mass index increase of 1.2 kg · m-2 (p=0.28) and the change in waist to hip ratio (p=0.31) were not statistically significant. M-value (mg. kg · min-1) did not change after testosterone therapy (5.86 [0.72] vs 5.29 [0.82], p=0.62). Insulin levels (mU · L-1) achieved during the clamps were 89.5 (14.2) before and 146 (32.2) after androgen therapy (p=0.127). There was no change in glucose area under curve (mg · min · dL-1) (14406 [502.2] vs 12557 [826.5], p=0.312). On testosterone replacement therapy total and LDL cholesterol levels (mg · dL- 1) declined (122.5 [13.4] vs 91.6 [5.0], p=0.04; 65.9 [9.9] vs 39.4 [7.3], p=0.05); Ratio of total cholesterol to HDL ratio also decreased significantly (p=0.05). Changes of serum triglycerides (p=0.25) and HDL cholesterol (p=0.19) did not attain statistical significance. Conclusions: Insulin sensitivity does not decrease on testosterone replacement therapy of male subjects with idiopathic hypogonadotrophic hypogonadism. Testosterone replacement was associated with decrease in other cardiovascular risk factors.",
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T1 - Effect of testosterone replacement on whole body glucose utilisation and other cardiovascular risk factors in males with idiopathic hypogonadotrophic hypogonadism

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AU - Reddy, K. S.

PY - 1998

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N2 - Background: Excessive testosterone in males or estrogens in females could explain their differences in coronary heart disease event rates. As a contraceptive testosterone is likely to be used at large scale the role of testosterone in increasing the risks of coronary heart disease needs investigation. Aim: To look at the role of testosterone in development of insulin resistance and other cardiovascular risk factors. Design: Prospective, before-after study on ten male subjects with idiopathic hypogonadotrophic hypogonadism pre- and post-testosterone replacement therapy; outcome measure; anthropometry, lipoprotein profile and M value (whole body glucose disposal rates on standard hyperinsulinemic euglycemic clamp; at insulin infusion rate: 40 mU · m-2). Results: Pre-treatment serum testosterone was 0.43 (0.515) ng · ml-1 LH was 1.29 (0.08) IU · L- 1, and FSH was 1.54 (0.08) IU · L-1. None had glucose intolerance. After replacement testosterone levels increased to 9.4 ng · mL-1 (p = 0.005); weight increase of 5.0 kg (p=0.140), body mass index increase of 1.2 kg · m-2 (p=0.28) and the change in waist to hip ratio (p=0.31) were not statistically significant. M-value (mg. kg · min-1) did not change after testosterone therapy (5.86 [0.72] vs 5.29 [0.82], p=0.62). Insulin levels (mU · L-1) achieved during the clamps were 89.5 (14.2) before and 146 (32.2) after androgen therapy (p=0.127). There was no change in glucose area under curve (mg · min · dL-1) (14406 [502.2] vs 12557 [826.5], p=0.312). On testosterone replacement therapy total and LDL cholesterol levels (mg · dL- 1) declined (122.5 [13.4] vs 91.6 [5.0], p=0.04; 65.9 [9.9] vs 39.4 [7.3], p=0.05); Ratio of total cholesterol to HDL ratio also decreased significantly (p=0.05). Changes of serum triglycerides (p=0.25) and HDL cholesterol (p=0.19) did not attain statistical significance. Conclusions: Insulin sensitivity does not decrease on testosterone replacement therapy of male subjects with idiopathic hypogonadotrophic hypogonadism. Testosterone replacement was associated with decrease in other cardiovascular risk factors.

AB - Background: Excessive testosterone in males or estrogens in females could explain their differences in coronary heart disease event rates. As a contraceptive testosterone is likely to be used at large scale the role of testosterone in increasing the risks of coronary heart disease needs investigation. Aim: To look at the role of testosterone in development of insulin resistance and other cardiovascular risk factors. Design: Prospective, before-after study on ten male subjects with idiopathic hypogonadotrophic hypogonadism pre- and post-testosterone replacement therapy; outcome measure; anthropometry, lipoprotein profile and M value (whole body glucose disposal rates on standard hyperinsulinemic euglycemic clamp; at insulin infusion rate: 40 mU · m-2). Results: Pre-treatment serum testosterone was 0.43 (0.515) ng · ml-1 LH was 1.29 (0.08) IU · L- 1, and FSH was 1.54 (0.08) IU · L-1. None had glucose intolerance. After replacement testosterone levels increased to 9.4 ng · mL-1 (p = 0.005); weight increase of 5.0 kg (p=0.140), body mass index increase of 1.2 kg · m-2 (p=0.28) and the change in waist to hip ratio (p=0.31) were not statistically significant. M-value (mg. kg · min-1) did not change after testosterone therapy (5.86 [0.72] vs 5.29 [0.82], p=0.62). Insulin levels (mU · L-1) achieved during the clamps were 89.5 (14.2) before and 146 (32.2) after androgen therapy (p=0.127). There was no change in glucose area under curve (mg · min · dL-1) (14406 [502.2] vs 12557 [826.5], p=0.312). On testosterone replacement therapy total and LDL cholesterol levels (mg · dL- 1) declined (122.5 [13.4] vs 91.6 [5.0], p=0.04; 65.9 [9.9] vs 39.4 [7.3], p=0.05); Ratio of total cholesterol to HDL ratio also decreased significantly (p=0.05). Changes of serum triglycerides (p=0.25) and HDL cholesterol (p=0.19) did not attain statistical significance. Conclusions: Insulin sensitivity does not decrease on testosterone replacement therapy of male subjects with idiopathic hypogonadotrophic hypogonadism. Testosterone replacement was associated with decrease in other cardiovascular risk factors.

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