Knowing the hormones of satiety
To explain improved satiety with high protein diets dependent pathways are used two incretins:
- Glucose-dependent insulinotropic poly peptide (GIP)
- Peptide-1 glucagon-1 (GLP – 1).
These hormones are synthesized in the intestine and secreted from entero endocrine cells in the intestinal epithelium in response to nutrient loading orally, so play an important role in the regulation of glucose balance in healthy subjects and are responsible for 50-70% of insulin response to a meal.
Besides its insulinotropic action, GLP-1 inhibits glucagon secretion dependently glucose, which together with effects including inhibition of gastrointestinal motility can regulate appetite in response to a mixed meal (CH + protein + fat) and food intake. Increased gastric retention, decreases hunger and desire to eat and increases satiety.
In the same study, it is concluded that chronic exposure to this incretin mimetics leads to weight reduction in type 2 diabetic patients; and that, therefore, the process of gastric emptying could play an important role in the perception of hunger and satiety, mediated by this hormone.
In IIFYM Guide Sergio Espinar, we mention cholecystokinin (CCK) stimulates intestinal motor activity and significantly contributes to the inhibition of gastric emptying. This is a peptide hormone found in the brain and the gastrointestinal tract, whose release is stimulated by ingestion of dietary protein and digestion (hydrolysis).
It is now clear that CCK reduces food intake and meal size and induces satiety in a variety of mammalian species, including rats, monkeys and humans. Brennan et al. (2011) reported that hunger repressed in lean and obese subjects after foods high in protein, is potentially mediated by CCK and ghrelin, leptin and insulin together.
Peptide YY (PYY)
As we have said, neuropeptides intestinal secretion inducing satiety, GLP-1, CCK, and, now, peptide YY (PYY) appears to be increased in response to a high protein diet.
These intestinal neuropeptides were greater following a high protein diet (30% P + 40% CHO + 30% F) compared with a moderate protein diet (10% P + 60% CHO + 30% F), which approximates more “recommendations” of health organizations.
Likewise, its relationship with ghrelin is present in increased satiety due to decreased levels of ghrelin postprandial response to a high protein breakfast compared with noncaloric high carbohydrate breakfast.
In this situation, it seems clear that one of the primary causes of overweight is likely to be a decrease satiety to follow recommended health organizations that continue to use the classic food pyramid, where CH are diets well over 50% of total daily.
Diets high in protein (> 20-25%) leading to reduction of energy intake at a subsequent meal, which is beneficial for weight loss via reduction of gastric emptying rate. This effect is not related to a conditioned taste aversion.