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Nathan Goodyear

Altered Cortisol Metabolism in Polycystic Ovary Syndrome: Insulin Enhances 5α... - 0 views

jcem.endojournals.org/...5907.long

PCOS PCO polycystic ovaries insulin IR resistance steroid 5-alpha reductase androgens

shared by Nathan Goodyear on 13 Mar 12 - No Cached
  • Nathan Goodyear on 13 Mar 12
     
    insulin, in women with PCOS, promotes increased 5-alpha reductase activity.  This results in a dysregulated HPA axis, promoting increased cortisol and androgen levels.
Nathan Goodyear

Oral contraceptive use and saliva diurnal pattern of metabolic ster... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25592051

oral contraceptives Testosterone DHEA cortisol contraception hormones

shared by Nathan Goodyear on 29 Jan 15 - No Cached
  • Nathan Goodyear on 29 Jan 15
     
    Oral contraceptives shown to reduce Testosterone and DHEA in women, but no effect on cortisol was seen.
Nathan Goodyear

Metabolic syndrome, hyperinsulinemia, and cancer | The American Journal of Clinical Nut... - 0 views

academic.oup.com/...4649276

metabolic syndrome cancer insulin insulin resistance hormones cortisol

shared by Nathan Goodyear on 10 Jan 21 - No Cached
  • Nathan Goodyear on 10 Jan 21
     
    Good review of insulin metabolic syndrome, insulin resistance, and cancer.
Nathan Goodyear

HPA axis changes during the initial phase of psychosocial stressor exposure in male mice - 0 views

joe.endocrinology-journals.org/...193.abstract

HPA stress cortisol pituitary metabolism hormone hormones

shared by Nathan Goodyear on 24 Jul 13 - No Cached
  • Nathan Goodyear on 24 Jul 13
     
    Stress response in a animal model is blunted at the level of pituitary through a decrease in ACTH release and through increase in peripheral metabolism
Nathan Goodyear

Tissue-Specific Increases in 11β-Hydroxysteroid Dehydrogenase Type 1 in Norma... - 0 views

www.ncbi.nlm.nih.gov/...PMC2795198

menopause 11-betaHSD1 11-betaHSD cortisol post-menopause post menopause women hormone hormones metabolism weight

shared by Nathan Goodyear on 29 May 14 - No Cached
  • Nathan Goodyear on 29 May 14
     
    11 beta HSD type 1 increases in menopause in normal weight women.  This may explain some of the metabolism changes seen in women post-menopause.
Nathan Goodyear

Acute Sleep Loss Induces Tissue-Specific Epigenetic and Transcriptional Alterations to ... - 0 views

academic.oup.com/...JC.2015-2284

sleep epigenetics BMAL1 CLOCK CRY1 PER1 sleep deprivation

shared by Nathan Goodyear on 30 Aug 17 - No Cached
  • Nathan Goodyear on 30 Aug 17
     
    Sleep deprivation, defined as 1 night of no sleep, changed epigenetic expression of BMAL via increased methylation. Other findings: decreased cortisol, increased glucose...
Nathan Goodyear

11β-HSD1 is the major regulator of ... [Proc Natl Acad Sci U S A. 2014] - Pub... - 0 views

www.ncbi.nlm.nih.gov/...24889609

11-betaHSD1 11-betaHSD adipose tissue obesity glucocorticoids cortisol

shared by Nathan Goodyear on 04 Jun 14 - No Cached
  • Nathan Goodyear on 04 Jun 14
     
    Study proposes that 11beta-HSD type 1 is the key to linking glucocorticoids and metabolic dysfunction.  The key point of this study is that it is the adipose tissue expression of 11beta-HSD type 1 that is the key.
Nathan Goodyear

Leptin and Androgens in Male Obesity: Evidence for Leptin Contribution to Reduced Andro... - 0 views

press.endocrine.org/...jcem.84.10.6082

obesity leptin low T low Testosterone Testosterone low T leydig cells LH leutenizing hormone men male hormones hormone

shared by Nathan Goodyear on 04 Sep 14 - No Cached
  • in male obesity basal and LH-stimulated androgen levels are reduced and inversely correlated with circulating leptin
  • functional leptin receptors are present in rodent Leydig cells
  • it is conceivable that in males high leptin concentrations may have a direct inhibitory effect(s) on Leydig cell function.
  • ...18 more annotations...
  • insulin is an important inhibitor of the synthesis of SHBG
  • no correlation between leptin and SHBG levels
  • SHBG reduction in obesity is a minor determinant of lowered androgen levels
  • SHBG can explain only up to 3% of the correlation
  • testicular T de novo production is impaired in obese men and that leptin seems to be the best hormonal predictor of this blunted response to LH stimulation
  • The low basal 17-OH-P levels found in massively obese men are consistent with a global impairment of Leydig cell steroidogenic function in this group of subjects.
  • These findings indicate that obese men have a FM-related defect in the enzymatic conversion of 17-OH-P to T, which is revealed by hCG stimulation.
  • Other studies have investigated the adrenal function in male obesity and have shown that basal cortisol and 17-OH-progesterone levels tend to decrease with the increase in the degree of obesity
  • High E2 can inhibit the expression and activity of the 17,20-lyase and may be responsible for this steroidogenic lesion
  • However, stimulated E2 levels were not higher in the obese than in controls, excluding the fact that the lower androgen response was due to an increased aromatization of T to E2 and that estrogens have a major role in the observed defect of 17,20-lyase activity in obese men.
  • the percentage increase in the 17-OH-progesterone to T molar ratio paralleled the increase in leptin levels of obese men
  • Multiple regression analysis indicated that the best hormonal predictor of the obesity-related reduction in T and FT basal levels and androgen changes after hCG stimulation was serum leptin concentration
  • insulin has no negative influences on androgen production in obese men
  • insulin is known to have stimulatory actions on T production that have been demonstrated in obese and normal weight men (57) and in Leydig cells in culture
  • the negative correlation between insulin and basal T can be partly explained by the inhibitory action of insulin on SHBG production
  • hypogonadal men have higher circulating leptin levels compared with hypogonadal patients under effective androgen substitution therapy
  • The impaired androgen response to LH stimulus was due to a defect in the enzymatic conversion of 17-OH-progesterone to T, which was disclosed by a leptin-related increase in 17-OH-progesterone to T ratio
  • Estrogens, which are inhibitory modulators of LH pulsatility and bioactivity
  • Nathan Goodyear on 04 Sep 14
     
    Leptin appears to be a good marker of low Testosterone.  This study proposes that the mechanism of action is potentially 2 fold: first, a decrease in LH release by leptin (kisspeptin?) and 2nd, a directed decrease in Testosterone production by the leydig cells in the testes.
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