A hypothalamus based enzyme has recently been shown to be “nutrient sensitive.” Researchers found that the enzyme SK6, when highly active, helps control appetite and weight gain.
Many topics of interest in neurological research have the tiny (“almond sized”) hypothalamus portion of the brain as a focal point. While the brain is a complicated and relatively poorly understood entity, significant evidence has accumulated linking the hypothalamus to the regulation of hunger, thirst, body temperature, energy, mood and circadian rhythms (internal body clock, responsible for sleep cycles and other phenomena). In a healthy individual, the hypothalamus regulates food intake by sensing the bodies energy storage (the majority through body fat), and sending neural signals to other parts of the body and brain to act accordingly through appropriate amounts of food intake. Ideally, an individual will therefore consume the number of calories necessary to healthily function, and not accumulate extra weight.
It’s been shown in past research that stimulation of certain parts of the hypothalamus increase appetite and food intake, linking a stimulated hypothalamus to weight gain. The mechanisms of this stimulation, or suppression (which would decrease appetite and food intake) are poorly understood, but the current study seems to have uncovered an explanation, in part, through the enzyme SK6.
SK6 (or p70 S6 Kinase 1) is an important enzyme that helps in the formation of cells, particularly nerve cells. The researchers first discovered that SK6 was “nutrient sensitive,” meaning that “S6K activity increases in the presence of carbohydrates and protein,” according to lead researcher Dr. Gary Schwartz. Being specifically responsive to food intake gave the possibility that SK6 could play a more prominent role on a bigger scale. Dr. Schwartz goes on to say that “this led us to believe that S6K might not only be involved in maintaining the structure and function of individual cells, but also in regulating the energy balance of the whole body.”
A virus was developed that raised and lowered SK6 activity in mice (mice, as well as all vertebrates, have a hypothalamus that plays a large role in many neural and metabolic functions), and was subsequently injected to observe the effect on appetite and food intake. The results were clear: “When we raised the activity of the enzyme, we saw reductions in food intake, in body weight, and in production of peptides that normally stimulate feeding. When we lowered SK6 activity, we saw essentially the opposite response,” says Dr. Schwartz. It’s noted that the reduction in food intake took place at each meal, but the desire to eat on a normal eating schedule was not hindered. In other words, the mice still wanted to eat as often as normal, they just wanted to eat less each time, which is a much healthier way of controlling weight than eliminating meals.
In further tests, it was shown that mice on high fat diets given SK6 activation, tended to eat less and gain less weight. This limited insulin resistance that often develops along with high fat diets and weight gain, and is a precursor to type 2 diabetes, and closely linked to heart disease.
The potential for the above studies findings is huge, though similar results must be found with humans before specific treatments can be developed. If SK6 does indeed play such a large role in food regulation in humans, “it may be possible to control obesity and other human metabolic disorders by developing drugs that regulate S6K activity,” concludes Dr. Schwartz.
Source: Defeat Diabetes Foundation: Schwartz, Gary. Heller, Michael. Cell Metabolism news release. December 2008.