Currently set to Index
Currently set to Follow
Skip main navigation

The Physiological Basis for Weight Regulation

Body weight regulation is influenced by multiple physiological processes so here's a list of major ones responsible for weight control.
Watch this lecture video to learn about how body weight is regulated.

Regulation of Body Weight Is Complex

Whilst regulation, or homeostasis, of body weight is most simplistically considered as an equilibrium between “Energy In” and “Energy Out”, the energy out regulation is extremely complex.
Three components of energy expenditure. Non-Resting Energy Expenditure 30%. Resting Energy Expenditure 60%. Thermal Effects of Feeding 10%.
In adults with a stable weight, Resting Energy Expenditure is the greatest contributor to energy output, between 60 and 70%.5 This is the energy expended on resting processes such as cardio-pulmonary activity.
Non-resting energy expenditure only accounts for 20-30% of energy output, and this relates to the energy expended during physical activity or non-sedentary behaviour. Hence it is important that when we think about exercise prescription for patients as part of their weight loss management plans, we understand this is a lesser component of the homeostasis equation compared to resting energy expenditure.
Finally, the thermal effects of feeding make up the remaining ~10% of energy expenditure.6

Central and Peripheral Processes Involved in the Homeostatic Regulation of Body Weight

For adults, despite wide variability in our day-to-day eating habits and physical activity, weight is maintained in a stable or narrow range for long periods of time. This is due to the central integration of peripheral signals about fat stores, energy intake, and longer-term energy stores.

Central Control

The primary brain region involved in appetite homeostasis is the arcuate nucleus of the hypothalamus, which projects to other brain regions such as the paraventricular nucleus and the lateral hypothalamus. Two interconnected groups of neurons in the arcuate nucleus have opposite effects on energy balance with some hormones increasing appetite and stimulating food intake and others suppressing appetite and inhibiting the drive for food.
However, it is evident that our desire to eat extends beyond a motivation for energy intake balance. The limbic system, our conscious will, and reward circuits all influence these central pathways.

Peripheral Control

Peripheral control of hunger and appetite is driven by hormonal signals generated from adipose tissue (leptin), the pancreas (insulin), and the stomach (ghrelin). These hormones travel through the bloodstream and via the vagus nerve to the brainstem and onto the hypothalamus and other areas of the brain including the area postrema and nucleus of the solitary tract. There are reciprocal pathways between these regions. Short term regulation of food intake is driven mainly by hormonal signals from the gastrointestinal system as follows:
Appetite increasing hormones: Ghrelin (produced in the stomach) is the major hunger-stimulating hormone) Appetite suppressing hormones: Glucagon-like peptide (GLP-1), amylin and peptide YY produced within the gastrointestinal tract
Long-term regulation of weight and appetite is driven by peripherally released hormones including LEPTIN (secreted by adipose tissue) and INSULIN (secreted by the pancreas). Under normal circumstances when an individual is in weight homeostasis, leptin is released proportionally to the volume of adipose tissue. Leptin travels to and acts on neurons in the brain to inhibit the neurons involved in the hunger stimulation pathways. Leptin is a key player in obesity, with experimental studies showing that pathological leptin deficiency or leptin resistance in the central nervous system results in severe obesity. Insulin is secreted by the pancreas and similarly acts to suppress appetite.
Image of brain. Inside the brain = Cerebral cortex (conscious will) -> Paraventricular nucleus (Oxytocin and CRH). Arcuate nucleus (NPY, CART, AgRP, aMSH)-> Paraventricular nucleus and Lateral Hypothalamus (Orexin. MCH). Paraventricular nucleus and Lateral hypothalamus -> Brain Stem. Brain stem -> Lateral Hypothalamus. NTS/Vagus -> Brain Stem. Leaving the brain Food intake and Energy expenditure. Stomach (Ghrelin) -> Hunger Stimulation. Gut (CCK, Oxnto-modulin, GLP-1, PYY3-36), Fat (Leptin), and Pancreas (Amylin, Insulin, PP) -> Hunger Inhibition
Figure: Simplistic summary of hormone interaction and central control of weight regulation. Modified from Proietto J. 2011. Medical Journal of Australia7
Use the points discussed in this video in your approach to weight management.
This article is from the free online

EduWeight: Weight Management for Adult Patients with Chronic Disease

Created by
FutureLearn - Learning For Life

Our purpose is to transform access to education.

We offer a diverse selection of courses from leading universities and cultural institutions from around the world. These are delivered one step at a time, and are accessible on mobile, tablet and desktop, so you can fit learning around your life.

We believe learning should be an enjoyable, social experience, so our courses offer the opportunity to discuss what you’re learning with others as you go, helping you make fresh discoveries and form new ideas.
You can unlock new opportunities with unlimited access to hundreds of online short courses for a year by subscribing to our Unlimited package. Build your knowledge with top universities and organisations.

Learn more about how FutureLearn is transforming access to education