Influence of residual insulin secretion and duration of diabetes mellitus on the control of luteinizing hormone secretion in women

Volpi,; Chiodera,; Gramellini,; Capretti,; Caffarri,; Speroni,; Vescovi,; Coiro,

doi:10.1046/j.1365-2362.1998.00367.x

Cited by 5 publications

(2 citation statements)

References 43 publications

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“…The hyperglycemia and insulin deficiency that occurs in patients with insufficient metabolic control have a negative effect on gonadotropin secretion . Insulin deficiency leads to diminished expression of kisspeptin1, a neuropeptide that has a key role in stimulating the secretion of hypothalamic GNRH .…”

Section: Discussionmentioning

confidence: 99%

Testicular function during adolescence in boys with type 1 diabetes mellitus (T1D): absence of hypogonadism and differences in endocrine profile at the beginning and end of puberty

et al. 2013

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Section: Discussionmentioning

confidence: 99%

Testicular function during adolescence in boys with type 1 diabetes mellitus (T1D): absence of hypogonadism and differences in endocrine profile at the beginning and end of puberty

et al. 2013

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“…Actions are clearly directed at several sites along the brainpituitary-gonadal axis and mediated through a number of diverse mechanisms (2,4,7,10,14). However, the effects of hyperglycemia specifically were shown, in several studies, to act at the pituitary and reportedly involve reduced responses to stimulation by GnRH (5,18,19).…”

mentioning

confidence: 99%

Sensitivity of pituitary gonadotropes to hyperglycemia leads to epigenetic aberrations and reduced follicle‐stimulating hormone levels

et al. 2018

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The connection between metabolism and reproductive function is well recognized, and we hypothesized that the pituitary gonadotropes, which produce luteinizing hormone and follicle-stimulating hormone (FSH), mediate some of the effects directly via insulin-independent glucose transporters, which allow continued glucose metabolism during hyperglycemia. We found that glucose transporter 1 is the predominant glucose transporter in primary gonadotropes and a gonadotrope precursor-derived cell line, and both are responsive to culture in high glucose; moreover, metabolite levels were altered in the cell line. Several of the affected metabolites are cofactors for chromatin-modifying enzymes, and in the gonadotrope precursor-derived cell line, we recorded global changes in histone acetylation and methylation, decreased DNA methylation, and increased hydroxymethylation, some of which did not revert to basal levels after cells were returned to normal glucose. Despite this weakening of epigenetic-mediated repression seen in the model cell line, FSH β-subunit ( Fshb) mRNA levels in primary gonadotropes were significantly reduced, apparently due in part to increased autocrine/paracrine effects of inhibin. However, unlike thioredoxin interacting protein and inhibin subunit α, Fshb mRNA levels did not recover after the return of cells to normal glucose. The effect on Fshb expression was also seen in 2 hyperglycemic mouse models, and levels of circulating FSH, required for follicle growth and development, were reduced. Thus, hyperglycemia seems to target the pituitary gonadotropes directly, and the likely extensive epigenetic changes are sensed acutely by Fshb. This scenario would explain clinical findings in which, even after restoration of optimal blood glucose levels, fertility often remains adversely affected. However, the relative accessibility of the pituitary provides a possible target for treatment, particularly crucial in the young in which hyperglycemia is increasingly common and fertility most relevant.-Feldman, A., Saleh, A., Pnueli, L., Qiao, S., Shlomi, T., Boehm, U., Melamed, P. Sensitivity of pituitary gonadotropes to hyperglycemia leads to epigenetic aberrations and reduced follicle-stimulating hormone levels.

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Diabetes: a metabolic and reproductive disorder in women

Thong

Codner

Laven

et al. 2020

The Lancet Diabetes & Endocrinology

123

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Influence of residual insulin secretion and duration of diabetes mellitus on the control of luteinizing hormone secretion in women

Cited by 5 publications

References 43 publications

Testicular function during adolescence in boys with type 1 diabetes mellitus (T1D): absence of hypogonadism and differences in endocrine profile at the beginning and end of puberty

Testicular function during adolescence in boys with type 1 diabetes mellitus (T1D): absence of hypogonadism and differences in endocrine profile at the beginning and end of puberty

Sensitivity of pituitary gonadotropes to hyperglycemia leads to epigenetic aberrations and reduced follicle‐stimulating hormone levels

Diabetes: a metabolic and reproductive disorder in women

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