#15 More bioscience! This time I will attempt to explain caloric homeostasis.

Sorry for any typos and while I did try to approach the ‘Pretend you’re explaining to a Martian’ method, I’m sure it veered away from that quite early on. 

This is going to be an explanation on caloric homoeostasis. Calories are the measure of the amount of energy in food. Whereas homeostasis is a property of a system in which variables are regulated so that internal conditions remain stable and relatively constant. It is the ability of the body to maintain adequate but not excessive energy stores and what prevents us from becoming obese. Two hormones play a key role in this process – leptin and adiponectin. They are both secreted by adipose tissue and work together with insulin (a hormone that regulates blood glucose levels) to regulate caloric homeostasis. Essentially, the equation for this process is energy consumed = energy expended + energy stored. So the amount of energy taken in is equal to the amount of energy used and stored by the body. This is because energy doesn’t run out, it is merely converted to different forms. If more energy is consumed than expended the outcome will be overweight or obesity.

Obesity is classified as having a body mass index (BMI) that is more than 30kg/m2, whereas an overweight individual has a BMI of more than 25kg/m2. When an individual is overweight/obese it means that they have excess fat stored in adipocytes (fat cells of the adipose tissue) as triacylglycerides (chains of fatty acids). There is a fixed number of adipocytes in adults meaning that the excess fat will merely cause them to swell in size. They can grow up to a thousand times their original size and this is what we see when looking at an obese/overweight individual. If more food is consumed than needed, the excessive calories will be stored as fat.

Obesity is considered an epidemic, especially in developed countries. In the US alone up to 30% of all adults are obese. This is not a good statistic because obesity is a risk factor in serious condition such as cardiovascular disease (CVD), diabetes mellitus and hypertension (high blood pressure). The reason why it is an epidemic is because of evolution. In the past bodies were programmed to quickly store excess calories was food was readily available. There were no supermarkets or restaurants then so food was eaten when it was present and the calories kept people going when it was sparse. Another reason is that we no longer face the threat of being eaten by another animal! In the past, fatter individuals were more likely to be killed and consumed whereas lean individuals were seen as not being rich enough. These days remaining lean is less beneficial. Genetic studies have also shown that obesity could be inherited.

The brain plays a key role in regulating this process. It releases biochemical signals that may be short or long term. Short term signals are active during meals where as long term signals provide an overall energy status of the body). These signals come from the gastrointestinal tract (tube that runs from the mouth to the anus), B cells of pancreas and fat cells and they all target the brain, and specifically a group of cells in the hypothalamus [part of the brain that governs physiological functions] called the arcuate nucleus. Signals from the GIT induce feelings of fullness – or satiety. This is relayed via short term signals from the gut to regions of the brain and reduces the urge to eat. One of the best studied short signals is cholecystokinin (CCK).

CCK is a family of peptide hormones secreted into the blood by cells in the small intestine, specifically the duodenum and jejunum. Their release is the satiation signal. CCK binds to its receptor which is a G-Protein Coupled Receptor (GCPR). This triggers a signal transduction pathway in the brain that generates feeling of satiety. CCK has an important role in digestion and it stimulates the secretion of pancreatic enzymes and bile salts from the gallbladder.

Another short term signal is glucagon-like peptide 1 (GLP1), which is secreted by intestinal L cells and located in the lining of the GIT. GLP1 binds to the GLP-1 receptor which is also a GCPR. It induces feelings of satiety and inhibits further eating by potentiating glucose induced insulin secretion by the beta cells of the pancreases while also inhibiting glucose secretion. Other signals are thought to exist but most of the ones identified so far are appetite suppressants – they inhibit further eating by decreasing appetite. In contrast, there are also appetite stimulators such as Ghrelin which acts on regions of the hypothalamus to increase appetite before a meal. It increases before a meal and then decreases afterwards. This property means that could be target for anti-obesity drug.

They are key signal molecules and regulate caloric homoeostasis over a time scale of hours/days. Leptin is secreted by adipocytes and insulin is secreted by beta cells of pancreas. Leptin is known as the “satiety hormone,” because it helps to regulate energy balance by inhibiting hunger. Leptin and insulin bind to receptors in arcate nucleus (ARC) of hypothalamus. ARC is involved in control feeding behaviour/secretion of various pituitary releasing hormones. Appetite is complex process and results from integration of multiple signals at hypothalamus. The presence of leptin/insulin will inhibit neurons which express appetite-stimulating peptides NPY (neuropeptide Y) and Agouti-related peptide [AgRP. Falling levels of leptin and insulin will activate these neurons and thus, decreased levels of leptin and insulin leads to increased food intake.


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