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When I was waiting to see my cardiologist for my 3-monthly appointment today, I met with a woman who came for her yearly checkup. Apparently, she has been diagnosed with diabetes mellitus type 2, atherosclerosis and chronic hypertension for quite some time. I have the opportunity to speak with her regarding her illnesses, and one of the thing that I've found out is that she can't control her urges to eat. She's morbidly obese, and I understood from that point, which could potentially cause by her uncontrolled urges to eat. In this article, I would like to share some of the known facts why is it people like this woman experienced intense hunger even with a lot of fat cells dangling around their waist. It's all come down with a hormone which we called as insulin.

Insulin is an anabolic hormone, and unlike its antagonist, glucagon which is also being secreted by the pancreas, insulin can reduce the amount of blood sugar in the systemic circulation by aiding its way into the cell to be used as an energy source or even being stored by the liver and muscle as glucagon. After a while, when all of the sites above have been fully occupied, all of the excess glucose would be converted into fat cells in a process called de novo lipogenesis (new fat making). Glucose can be obtained either by:

• Eating carbohydrate
• Gluconeogenesis (production of glucose from a non-carbohydrate source like protein)
• Glycogenolysis (production of glucose from glycogen by the action of glucagon)

Now we know that glucose will be converted into a fat cell if all of the available room in the cell is full. Glucose can't stay in the blood circulation as it can cause the production of advanced glycation end product (AGE) which has a damaging effect towards cellular component which will cause further harm. So fat cell is the last resort to store any excess glucose, and that's how eating carbohydrate, not fat can cause you to become fat.

Why fat people get hungry all the time

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If we think logically, fat is a form of energy. If you're familiar with high-intensity interval training (HIIT), you will know that for the first 20 minutes, or so our body energy requirement was supplied by glucose, but after that, your glucose store will become depleted. Fat cells will take over and provide energy for the rest of the workout session so technically; fat cells give a whole lot of energy. Now let's consider obese people, they have a lot of fat cells. If a human is a machine, then we can say that obese people lives surrounded by a lot of oil or batteries to operate the device, but why do fat people have an intense hunger and compulsion to eat when they have so much more available energy?

The key lies in the hormone which is responsible for converting the fat cell into energy when the body runs out with one. This hormone is called a hormone-sensitive lipase (HSL). HSL, as indicated by its name is sensitive to insulin which a hormone responsible for converting or storing glucose as energy so when the body has a lot of insulin, HSL will not be activated. It's like saying that, insulin is currently at work which means, there are a lot of potentials substrate that can be used as an energy source, so there is no need to mobilise fat cells. It would be counterproductive.

The thing is, there is such thing as pre-meal insulin secretion which is triggered by the pancreas when we are in a situation that our body will expect us to get some food. For example, you are a student who is currently sitting in a lecture hall waiting for the lecture to be over so that you can go back and do some stuff. After your class has finished, you walk past the cafeteria, and you can smell the food that is cooked. Suddenly, you felt hungry even though just 5 seconds ago, you were not. The hunger can be caused by two potential factors:

• An Increase of pre-meal insulin secretion by the pancreas
• Increase in the hunger hormone secretion called ghrelin
• Decrease readability of Leptin by the brain due to a high level of insulin

The role of leptin hormone in satiety

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Some terminologies might be confusing in the statement above. Leptin is a satiety hormone, while ghrelin is a hunger hormone. I think you can predict their function based on their description; it's quite straightforward. Ghrelin is motivated by secretion of insulin while leptin is secreted by fat cells and if the brain doesn't have any problems of reading its signal, then we can say that we will feel full all the time. Now let us think; If leptin is being secreted by a fat cell which would make us feel full, doesn't that means an obese people who be satiated all the time? Why do they keep on consuming more food to feel satiated? The answer to that question is insulin can block the leptin signal to the brain which disrupts the biochemical sign of being satiated so we will keep on eating. Even with all of the profound logic, people who eat a lot of carbohydrates can still eat some other food later thanks to insulin. The amount of pre-meal insulin secretion would depend on our perception of the level of sweetness of a particular food. The sweeter the food, the higher the amount of pre-meal insulin will be secreted. It's like the body will prepare itself to process a whole lot of glucose thus forcing the pancreas to produce more. This is also why we felt hunger when the time of our usual meal is reached, e.g. breakfast, lunch and dinner. The body will expect you to eat some food so it will secrete insulin thus making you hungrier.

A few studies conducted recently have proved an association between the hunger hormone, ghrelin and insulin. So now, your insulin will not only decrease the efficacy of leptin to make your body feel satiated, but it also will make you feel hungrier no matter how much energy which is available in your body. It's unfortunate, but that's how a fat people will stay fat, and it will be difficult for them to reduce weight. There are a lot of weight-losing program out there which used insulin level as an essential factor to lose weight. Reduction of insulin will allow the body to use body fat as an alternative to the glucose shortage which can optimise function. Easier said than done; this would require a lot of motivation, support and willpower to achieve an ideal weight to stay healthy.

References and reading materials

• Chabot, F., Caron, A., Laplante, M., & St-Pierre, D. H. (2014). Interrelationships between ghrelin, insulin and glucose homeostasis: Physiological relevance. World Journal of Diabetes, 5(3), 328–341.
• Mlinar B, Marc J. New insights into adipose tissue dysfunction in insulin resistance. Clin Chem Lab Med. 2011;49:1925–1935.
• Miegueu P, St Pierre D, Broglio F, Cianflone K. Effect of desacyl ghrelin, obestatin and related peptides on triglyceride storage, metabolism and GHSR signaling in 3T3-L1 adipocytes. J Cell Biochem. 2011;112:704–714.
• Jade Teta (2012, February 8). Metabolic Effect. The Science of Insulin. Retrieved March 7, 2018, from https://www.metaboliceffect.com/science-insulin/