Oestrogen Decline and Its Impact on Energy Expenditure

Published February 2026 | Educational Resource

Overview of Oestrogen's Metabolic Role

Oestrogen is far more than a reproductive hormone. It is a metabolic regulator with profound effects on how the body processes, stores, and expends energy. Oestrogen receptors are distributed throughout tissues involved in energy metabolism, including skeletal muscle, adipose tissue, liver, pancreatic beta cells, and the hypothalamus.

During the reproductive years, oestrogen is produced primarily by the ovaries in a cyclical pattern. This consistent hormonal milieu maintains metabolic stability and supports efficient energy regulation.

Mechanisms of Oestrogen's Influence on Metabolism

Oestrogen exerts its metabolic effects through several pathways:

1. Thermogenesis and Heat Production

Oestrogen influences the expression of uncoupling protein 1 (UCP1) in brown adipose tissue and mitochondrial function in general. This affects thermogenesis—the production of heat as an energy expenditure mechanism. Declining oestrogen reduces basal thermogenic activity, lowering overall energy expenditure.

2. Appetite Regulation Centres

The hypothalamus contains high concentrations of oestrogen receptors. Oestrogen modulates the activity of pro-opiomelanocortin (POMC) neurons, which suppress appetite, and neuropeptide Y (NPY) neurons, which stimulate appetite. The balance between these systems influences hunger and satiety signals. As oestrogen declines, this balance shifts, potentially affecting appetite perception.

3. Insulin Sensitivity and Glucose Handling

Oestrogen enhances insulin receptor expression and improves insulin signal transduction in muscle and adipose tissue. Lower oestrogen levels correlate with reduced insulin sensitivity and increased fasting insulin levels. This impairs glucose uptake by cells and promotes greater insulin secretion in response to carbohydrate intake.

4. Fat Oxidation and Substrate Utilization

Oestrogen promotes the oxidation of fatty acids as a fuel source. This is partly due to oestrogen's effects on peroxisome proliferator-activated receptor gamma (PPARγ) and lipoprotein lipase activity. During perimenopause, reduced oestrogen shifts the balance toward greater carbohydrate dependence and reduced fat oxidation efficiency.

Adipose Tissue Remodelling

Beyond metabolic rate effects, oestrogen influences where fat is stored. Oestrogen promotes the deposition of fat in subcutaneous sites (under the skin, particularly in hips and thighs) and suppresses visceral (central, abdominal) fat accumulation. Oestrogen receptors in adipose tissue regulate this distribution.

As oestrogen levels decline, this regulatory influence diminishes. Adipose tissue loses the inhibitory signal for visceral fat deposition. Research demonstrates that postmenopausal women, on average, show relatively greater accumulation of central fat compared to premenopausal women of the same age and weight.

Age Interaction and Confounding Variables

It is important to note that women undergoing perimenopause are also experiencing age-related changes independent of hormonal shifts. Both age and oestrogen decline contribute to metabolic reductions. Some research attempts to parse these contributions by comparing women of similar age in different menopausal stages, or by tracking individual women longitudinally.

These studies collectively suggest that oestrogen decline accounts for a measurable but not total proportion of midlife metabolic reductions.

Summary

Oestrogen exerts broad metabolic effects through multiple physiological pathways. Its decline during perimenopause reduces thermogenesis, alters substrate utilization, shifts fat distribution patterns, and influences appetite signals. These changes interact with age-related metabolic declines to reshape energy balance during this life stage.

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