Yes, you read right. Flab is not always bad. Scientists have discovered that being a little overweight comes with quite a few benefits.
According to several studies, the much-maligned fat cells, the ones that many people jog, sprint, swim, and walk to melt away, boost our energy levels. These fat cells crosstalk with the brain, as was discovered in experiments on laboratory mice. Scientists also indicate that the presence of an optimum number of fat cells in the body enhances longevity and keeps away several age-related symptoms and disorders.
Fat Cells and the Brain
Although the common man continues to treat fat as bad, and fat cells as things to get rid of, scientists have been working with fat cells for several years to uncover their physiological roles and relevance. In an earlier experiment carried out on lab mice, it was found that the hormone leptin produced by fat cells carries information about the amount of energy stored in these tissues in the abdominal region to the central nervous system. Leptin, or the “satiety” hormone, stimulates the brain to trigger signals that suppress the need for taking food. So there is compelling evidence that fat cells in the body communicate with the brain and influence the latter’s actions.
Another study indicates that the hypothalamus region of the brain communicates with adipose or fat tissues and regulates various metabolic processes. According to the findings of this study, the mammalian hypothalamus houses a pacemaker of sorts that monitors and regulates various core biological processes like eating, metabolism of food, and the sleep/wake cycle. This is a 24-hour clock that also influences physical activity and energy levels in individuals.
There are several components like proteins BMAL1 and CLOCK that regulate the 24-hour clock and keep it ticking and working the way it should. BMAL1 and CLOCK are also present within fat cells. In the above-mentioned study carried out on laboratory mice, it was found that animals with mutant varieties of BMAL1 and CLOCK had wayward circadian clock rhythms. These animals also exhibited several metabolic disorders that developed when the normal functionality of the ß cells in the pancreas was hampered.
These landmark studies shed critical insights into the pathogenesis of metabolic diseases like type 2 diabetes. The findings from the above-mentioned studies also led scientists to think that having a bit of fat is not that bad, after all. Scientists believe that human beings can benefit significantly from having a body mass index that skims the lower end of the range that is usually considered to be overweight. We need fat to survive!
Fat: Its Effect on the Hypothalamus and Pancreas
According to recent studies, fat cells communicate with the hypothalamus. This region of the brain is responsible for aging, longevity, and maintaining the energy levels of the body. Additionally, the hypothalamus regulates heart rate, blood pressure, hunger, thirst, and the sleep/wake cycle.
The presence of fat cells optimized the functions of the hypothalamus leading to greater energy levels in individuals. The main player in this development is an enzyme nicotinamide phosphoribosyltransferase (NAMPT) produced by fat tissues. NAMPT is involved in production of NAD, one of the energetic substances in the cell that is responsible for maintaining optimal cellular functionality. The scientists discovered that adipose tissues typically produce large quantities of NAMPT and some of it end up in the bloodstream and gets transported to the brain.
In the course of this study, scientists discovered that when there was a lack of the NAMPT enzyme in the fat cells, there was also a considerable drop in the energy levels within the adipose tissues. Although other major organs and muscles of the body remained unaffected by the change in the levels of this enzyme, the hypothalamus exhibited a similar drop in energy levels.
There were also other developments when the amount of this enzyme dropped inside the fat cells and the hypothalamus. An increase in the energy levels of the hypothalamic cells also enhances the functionality of the SIRT1 protein. This protein has been linked to longevity in mice.
These findings should also interest people living with diabetes. Fat cells produce NAMPT, and NAMPT generates nicotinamide mononucleotide that stimulates pancreatic beta cells to churn out more insulin. Although pancreatic cells themselves produce NAMPT, the amount is not adequate. So the pancreas has to depend on the fat cells to supplement its production. So the fat cells also communicate with the pancreas to regulate the production of NAMPT.
However, researchers sound a note of warning. Obesity has been conclusively linked with the development of type 2 diabetes. It is evident that there is a limit up to which the NAMPT enzyme can go on enhancing the functionality of the pancreas. Once this limit is reached, the beneficial effects of NAMPT are negated.
It is evident that a certain amount of fat is necessary for the body to not only maintain its core physiological functions but also for its survival.
How Much Fat is Good?
The findings of the above-mentioned studies will surely interest weight-watchers, and it is natural for them to wonder how much fat is good for the body. Scientists do not yet have an exact answer to this question. They are, however, quick to warn that their findings should in no way be interpreted as a license to go on a binge-eating spree, cancel the gym membership, or stop going for the morning jog around the park. Being on either end of the underweight-morbidly obese spectrum is bad for you.
So here’s the lesson. If you were trying to lose weight, keep at it. But don’t resort to fad diets, starvation, and obsessive exercising to attain an unhealthy body weight. Being a little overweight has long-term benefits. And it is not really surprising that this phenomenon, like many other processes in the body, is linked to the way our brain functions.
References
Revollo, J., Körner, A., Mills, K., Satoh, A., Wang, T., Garten, A., Dasgupta, B., Sasaki, Y., Wolberger, C., Townsend, R., Milbrandt, J., Kiess, W., & Imai, S. (2007). Nampt/PBEF/Visfatin Regulates Insulin Secretion in ? Cells as a Systemic NAD Biosynthetic Enzyme Cell Metabolism, 6 (5), 363-375 DOI: 10.1016/j.cmet.2007.09.003
Yamada, T., Katagiri, H., Ishigaki, Y., Ogihara, T., Imai, J., Uno, K., Hasegawa, Y., Gao, J., Ishihara, H., Niijima, A., Mano, H., Aburatani, H., Asano, T., & Oka, Y. (2006). Signals from intra-abdominal fat modulate insulin and leptin sensitivity through different mechanisms: Neuronal involvement in food-intake regulation Cell Metabolism, 3 (3), 223-229 DOI: 10.1016/j.cmet.2006.02.001
Yoon, M., Yoshida, M., Johnson, S., Takikawa, A., Usui, I., Tobe, K., Nakagawa, T., Yoshino, J., & Imai, S. (2015). SIRT1-Mediated eNAMPT Secretion from Adipose Tissue Regulates Hypothalamic NAD+ and Function in Mice Cell Metabolism, 21 (5), 706-717 DOI: 10.1016/j.cmet.2015.04.002
Yoshino, J., & Imai, S. (2010). A Clock Ticks in Pancreatic ? Cells Cell Metabolism, 12 (2), 107-108 DOI: 10.1016/j.cmet.2010.07.006
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