Fat Biochemistry: Tweak the Wrong Perception

Fat requires a profuse supply of blood from the capillaries, thus, putting a tension to the cardiovascular system. It causes wear on the joints and its accumulation interferes with breathing when muscles relax.

Studies for the cure of obesity have been failing for decades, partly because doctors often weigh it with voracity. However, fat is now a distinct organ that could send two general kinds of messages to different parts of our body either: “I am full” or “I need more.”

Fat cells are tiny spheres that require a million of them to store calories; yet, it is a non-stop factory for absorption and release of substances to respond to the body’s needs. When calorie intake exceeds, fat cells swell to as much as six times its minimum size and multiply from 40 billion to 100 billion. Losing weight causes them to shrink in size but their number decreases slowly.

Also known as white adipose tissue (WAT), white fat cells are the most commonly known fat cells. An average lean person has roughly 20 to 40 billion WAT and an obese has ten times more.

WAT provides heat insulation that stores reserve energy. It affords cushioning from shock and jarring. But an excessive amount does not give any benefit at all.

The less common fat cells are the ones that disappear by adulthood – brown adipose tissue. It maintains body temperature, generates heat, and burns calories without physical motion. It sits within a web of capillaries that communicate heat and energy throughout the body. Both kinds contribute an important thing to our body.

Fat biochemistry has the traces to its tenacity and to the diseases associated with obesity, including cancer, diabetes, and heart diseases. Consequently, it holds the body’s natural solution to losing weight.

Research developments showed that adipose tissue is not simply a depot for lipids but also an endocrine organ that plays a vital function in the integration of metabolic and inflammatory signals for the control of energy homeostasis. Proteins secreted from that tissue, collectively named adipocytokines, include leptin, tumor necrosis factor (TNF), plasminogen active inhibitor type 1 (PAI-1), resistin, and adiponectin.

TNF, Resistin, Adiponectin, PAI-1

Diabetes is the buildup of glucose in the blood, so the usual idea is diet: that people get diabetes because they are fat because they consume too much sugar. However, researchers now believe that the origin of diabetes lie in part with fat biochemistry.

TNF causes inflammation which is a risk to the heart. On the other hand, PAI-1 blocks the body’s own clot-busters, a detriment in the case of strokes.

TNF and resistin interferes with the operation of insulin. Now, we know for a fact that insulin resistance is a precursor of full blown diabetes. Aside from that, resistin apparently promotes the conversion of fatty acids into glucose by the liver, a process useful if you are temporarily out of food, but a hazard if you have diabetes.

However, adiponectin reacts the opposite way. It appears to be a modulator of insulin action. It significantly increases insulin sensitivity as well as anti-inflammatory properties that include suppression of macrophage phagocytosis and TNF secretion. Although it is only produced by adipose tissue, its levels are paradoxically less in obese than in lean humans. Unfortunately, the fatter you are, the more resistin you make, and the less adiponectin.

Leptin, Fatty Acids

One of the recent conceptual breaks is the discovery that fat cells behave in different parts of the body; therefore, fat distribution has an implication on a person’s health. Fat carried in the hips and the thighs is considered benign as compared to those accumulated around the organs in the abdomen. Those in abdominal parts are the visceral fats that produce more inflammatory and clot-promoting compounds. It is the first to disappear during exercise.

However, too much stress could still lead you to become fatter. Cortisol is a catabolic hormone produced by the adrenalin glands. It acts as a normal analgesic. But cortisol has a negative effect on protein synthesis. High levels of cortisol are concurrent with the loss of muscle tissue. This is a double edged sword, for if you lose muscle, your metabolic rates drop and fat levels will increase. Also, fatty acids convert inactive cortisol to active ones. Active cortisol promotes fat deposits in the abdomen, producing visceral fats. In addition, these fats are not susceptible to liposuction, only the subcutaneous ones.

Researchers tried to find the shortcut to losing weight. The discovery of leptin in 1994 by Jeffrey M Friedman led to hopes that peptide could be used to treat obesity. Leptin is an appetite-suppressing hormone. It speeds metabolism and burning calories. The more fat cells, the more leptin produced, signaling the brain to stop food intake. However, it soon emerged that most obese people are resistant to it rather than deficient in it. The resistance is associated with the loss of function at several stages of the leptin-signaling pathway. This leptin resistance still needs a lot of demonstration to find answers.

Although there are compounds produced by fats that could naturally control body weight, still, the body has many overlapping systems in arrays of negative and positive loops. Example is the hormone ghrelin, which sends the signal to the brain to eat whenever the stomach is empty.

Fat, though, has so far refrained from chemical assaults, with the result that more people are reduced to gastric bypass surgery. That is why the most practical solution now is dieting – eat less, exercise more (Written With Joan Kristi Decena Zaldivar).