When examining the effects of leptin on the human body, most people are primarily interested in its effect regarding weight reduction, rather than some of its other lesser known general biological functions. Indeed, it was leptin’s role in regulating energy intake in the body that led to leptin’s initial discovery, as well as the vast bulk of the research efforts aimed at comprehending its physiological effects and the way it can be managed through external factors.
To bring matters down to an overly-simplified level, leptin operates in conjunction with two other significant hormones in the body, as far as energy intake is concerned. Leptin itself is often referred to as the “satiation hormone”, which means that it serves as a sort of “off-switch” to the central part of the brain. This off-switch function signals the brain that the body is sufficiently fueled up, and can therefore operate its full range of functions without interruption or reduction. Metabolism rates are ratcheted up to their highest level, the desire for additional caloric intake is suppressed, and mental processes operate at peak efficiency.
What one might call leptin’s twin, Ghrelin, is a collection of cells in the midsection of the body that sends the opposite signal to the brain—namely, that energy intake is below the current level of energy conversion and thus the body needs to dial down its metabolic rates and hurry up with the gravy. Put simply, one signal says “I’m full” and one signal says “I’m hungry.”
Leptin is not alone in its struggle with Ghrelin cells, however. It has a sidekick in the form of the hormone amylin, which assists in signaling the brain that the body is stoked up and ready to go. The reason these two hormones are regarded with such hope as far as obesity treatment goes, is that amylin has shown promise in its ability to overcome the great perceived weakness of leptin.
That weakness lies in the fact that the body, under certain conditions, starts to “turn off” its response to the signal provided by leptin. Physiological changes, such as the onset of diabetes and high triglyceride levels, can cause the body to develop a resistance to leptin, which renders ineffective any therapy in the form of externally-supplied leptin to attempt to boost circulating levels in the body.
The brain simply doesn’t listen, even when leptin is shouting with highly-increased levels. Amylin appears to partially restore the body’s response to leptin, at least in clinical trials involving obese mice, and thus the duo offers some hope of finally creating a clinical treatment for the physiological impact of obesity, rather than continuously operating on the mental and psychological level.
The interaction of these three hormones – leptin, ghrelin and amylin- shows that there are definitely genetic factors to obesity which can be exacerbated by dietary and lifestyle choices, but are nevertheless subject to pharmaceutical control. Additionally, leptin is important in the Venus Factor weight loss program. Of course such a regimen needs to be combined with an effort to get those factors which help turn off leptin signals, such as Type-2 diabetes and elevated triglyceride levels in the bloodstream, back into balance as well. In the following video, a nutrition expert discusses how to keep these three hormones balanced.