Appetite Regulation Signals in Perimenopausal Phase

Published February 2026 | Educational Resource

The Neuroendocrine Control of Appetite

Appetite—the desire to eat—and satiety—the satisfaction after eating—are regulated by integrated neuroendocrine signals. Multiple hormones and neuropeptides communicate information about energy status, nutrient availability, and gut fullness to appetite control centres in the hypothalamus. The balance between appetite-promoting and appetite-suppressing signals determines hunger intensity and eating behaviour.

Key Appetite Regulation Hormones

Ghrelin: The "Hunger" Hormone

Ghrelin is produced primarily by the stomach in response to fasting. It crosses the blood-brain barrier and stimulates appetite by activating neuropeptide Y (NPY) and agouti-related peptide (AgRP) neurons in the hypothalamus. Ghrelin levels rise before meals and fall after food intake. Oestrogen suppresses ghrelin secretion, reducing hunger signals.

During perimenopause, declining oestrogen may permit higher ghrelin levels, potentially increasing appetite perception.

Leptin: The "Satiety" Hormone

Leptin is produced by adipose tissue in proportion to total body fat stores. It signals energy abundance to the hypothalamus, suppressing appetite. Leptin activates pro-opiomelanocortin (POMC) neurons, which produce alpha-melanocyte-stimulating hormone (α-MSH), a potent appetite suppressant.

Oestrogen enhances leptin sensitivity in appetite control centres. With declining oestrogen, leptin signalling may be blunted, reducing the suppressive effect of leptin on appetite despite adequate or elevated leptin levels—a state termed leptin resistance.

Peptide YY and GLP-1: Satiety Signals

Peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) are released by intestinal L-cells in response to nutrient intake, particularly fat and protein. These hormones signal the hypothalamus that food has been consumed and promote satiety. Both are modulated by oestrogen.

Cholecystokinin: Post-Meal Satiety

Cholecystokinin (CCK) is released by the duodenum in response to dietary fat and protein, promoting fullness and reducing meal size. Oestrogen enhances CCK sensitivity in appetite control centres.

Oestrogen's Role in Appetite Regulation

Oestrogen receptors are abundantly expressed in hypothalamic appetite centres. Oestrogen has multiple effects on appetite control:

• Suppresses ghrelin production and hypothalamic ghrelin sensitivity
• Enhances leptin and other satiety hormone signalling
• Promotes POMC neuron activity (appetite suppression)
• Suppresses NPY/AgRP neuron activity (appetite promotion)
• Increases perceived satiety after eating

Overall, oestrogen is anorexigenic—it promotes appetite suppression and eating restraint.

Changes During Perimenopause

As oestrogen declines during perimenopause, the balance of these appetite signals shifts:

• Reduced ghrelin suppression may increase hunger signals
• Blunted leptin and satiety hormone signalling may reduce fullness perception
• Shift toward relatively greater NPY/AgRP (appetite-promoting) activity
• Potential increase in subjective appetite and eating motivation

However, individual variation is substantial. Not all women experience increased appetite during perimenopause; some report decreased appetite or no change.

Appetite Changes and Energy Balance

Changes in appetite perception during perimenopause interact with the reduced energy expenditure described in other articles. If energy expenditure declines by 5–10% but appetite-suppressing signals also decline, the net effect on energy balance is compounded. Women maintain or increase their usual energy intake while expenditure falls, creating energy surplus and promoting energy storage.

Interaction with Other Perimenopausal Symptoms

Appetite regulation during perimenopause is also influenced by other concurrent symptoms:

• Sleep disruption: Poor sleep increases ghrelin and decreases leptin, promoting appetite
• Mood changes: Depression and anxiety alter appetite regulation through distinct neuroendocrine pathways
• Hot flashes: May trigger eating behaviours as coping mechanisms
• Stress: Activates cortisol production, which influences appetite and fat storage

Individual Variation in Appetite Changes

Factors influencing the magnitude of appetite signal changes include:

• Genetic predisposition to appetite sensitivity
• Rate of oestrogen decline (rapid vs. gradual)
• Baseline leptin sensitivity and metabolic health
• Concurrent presence and severity of other perimenopausal symptoms
• Dietary composition (high-protein diets may enhance satiety despite hormonal changes)

Summary

Appetite and satiety are controlled by integrated neuroendocrine signals in which oestrogen plays a major regulatory role. During perimenopause, declining oestrogen shifts the balance toward relatively increased appetite-promoting signals and reduced satiety perception. These changes, combined with metabolic rate reduction, create a physiological context promoting energy storage.

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