Role of Ovarian Hormones in the Long-Term Control of Glucose Homeostasis Glycogen Formation and Gluconeogenesis

Abstract

The effect of ovarian hormones on in vivo gluconeogenesis and glycogen deposition in liver, uterus, skeletal and cardiac muscle was studied. Ovariectomized adult female mice were treated with replacement doses of estradiol, progesterone, both hormones combined, or vehicle only for 15 weeks. Compared with intact control mice, ovariectomy increased gluconeogenesis and reduced the glycogen content of all tissues examined. Treatment with estradiol and progesterone, individually and in combination, increased tissue glycogen deposition. Estradiol alone consistently produced the greatest effect, except on hepatic glycogen, which was maximally increased by the combined estradiol-progesterone regimen. Estradiol markedly reduced gluconeogenesis, and this effect was antagonized by progesterone. The results indicate that the lower plasma glucose concentrations produced by ovarian steroids result in part from reduced glucose neoformation and greater storage of glycogen in liver and muscle tissues.

A 1HNMR-Based Metabonomics Study of Postmenopausal Osteoporosis and Intervention Effects of Er-Xian Decoction in Ovariectomized Rats

“…It has been reported that ovariectomy and etrogen deficiency led to decreased energy expenditure[27], increased glucose level and increased visceral adipose tissue [34,35]. Long-term estrogen deficiency may lead to reduction of insulin secretion, thus weakening the ability of controlling glucose level in ovariectomized rats [26].…”

Effects of Estradiol on Glycemic and CNS Neuronal Activational Responses to Recurrent Insulin-Induced Hypoglycemia in the Ovariectomized Female Rat

“…Estrogenic modulation of IIH may reflect control of sensory signaling of glucopenia, magnitude and/or duration of physiological and behavioral motor responses to hypoglycemia, and/or peripheral actions of insulin and counterregulatory hormones on target tissues. Indeed, OVX is reported to decrease glucose tolerance [13], and enhance hyperglycemic actions of glucagon and epinephrine [12], in part by suppression of hepatic glycogen production and stimulation of gluconeogenesis [14]. The current evidence that RIIH exacerbates effects of insulin in oil- but not E-implanted OVX rats implies that functions underlying glucostatic regulatory mechanisms or glucose production, storage, and/or utilization become adapted to recurring glucoprivation in the absence of circulating estradiol.…”

Genetic Basis for Sex Differences in Obesity and Lipid Metabolism

“…Assessments of insulin resistance show greater occurrence in men than women, even after adjusting for age and body mass index (42, 59, 80, 86). Key mechanisms that have been implicated include effects of gonadal hormone-dependent and -independent sex differences in regional adipose tissue distribution, production of cytokines and adipokines, hepatic gluconeogenesis and glycogenolysis, and glucose uptake by skeletal muscle (1, 86, 102). Sex differences in the mechanisms of dysglycemia raise a concern that diagnosis of MetSyn based on fasting glucose levels may not reliably identify women that have MetSyn and should undergo some intervention.…”