Weight management is the result of the balance between energy intake and energy consumption. The ingredient DNF-10® promotes weight loss by regulating the mediators of satiety, as various clinical studies prove.
What is DNF-10®?
DNF-10® is a patented food-based ingredient obtained from a screening of low molecular weight peptides after proteolysis of saccharomyces cerevisiae. Saccharomyces cerevisiae (beer yeast, also known as baker’s yeast, brewer’s yeast or wine yeast) is the most commonly used yeast. The yeast is used for fermenting carbohydrates. Studies prove that DNF-10® improves the feeling of satiety and reduces food intake.
The main results of the double-blind, randomized and placebo-controlled clinical trials with a total of 134 subjects:
- Significant reduction in calorie intake from the first week.
- Considerable weight loss after the first month.
- Weight loss due to fat mass.
- Abdominal fat considerably reduced.
- Waist circumference reduced by 5 cm.
After taking DNF-10® for two months, 80% of the subjects thought less of food during the day than at the start of the supplement. The subjects also reduced their calorie intake by 600 calories a day after two months.
Ghrelin and leptin
DNF-10® promotes weight loss through a regulation of the mediators of satiety. Saturation and appetite are caused by modulation of our levels of ghrelin and leptin. DNF-10® acts as a satiety agent in that it reduces the production of ghrelin. A few hours after our last meal, a slight feeling of hunger starts, which increases over time as the glycemia (blood sugar) lowers. At the same time, after the digestion process when our stomach empties, it secretes ghrelin, “the hunger hormone”. Ghrelin is a peptide hormone produced in the gastrointestinal tract, which functions as a neuropeptide in the central nervous system. The action of ghrelin will progressively supersede the effect of leptin, known as “the hormone of energy expenditure”. Indeed, leptin acts as a mediator of long-term regulation of energy balance. Leptin is released into the circulatory system by the adipose tissue as a function of energy stores: the more adipose tissue the more leptin secretion.
All these mediators, associated with the exposure to food, generate the secretion of hypothalamic neuropeptides like neuropeptide Y (NPY), which is involved in physiological and homeostatic processes in both the central and peripheral nervous systems. This chain reaction leads to our next food intake, and to unhealthy eating choices when unbalanced.
All these physiological pathways leads to food intake and then the food arrives in the digestive system. The distention of the stomach inhibits the release of ghrelin; the increase of our glycemia leads to an increased production of insulin and as food moves down to our intestine, it stimulates the release of the neuromodulators such as CCK, or PYY, promoting satiation.
While we eat there is a negative feedback to the brain, with satiety as a finality, leading to inhibition of further eating, decline in hunger and increase in fullness after a meal is finished.