High protein diet has proven mechanisms that lead to weight loss
Date: January 19th, 2006
Title: “Protein, satiety power, and body weight”
Speaker: Daniel Tomé
The precise role of different macronutrient combinations, i.e. the relative effect of carbohydrate, fat and protein on total energy intake, energy nutrient metabolism and adiposity, remains a subject of debate. The level and quality of protein in the diet influences food and energy intake.
Mechanisms of protein influencing food intake:
- The existence of an aversion response to diets deficient in or devoid of protein or deficient in at least one essential amino acid;
- The existence of a mechanism that enables attainment of the minimum requirement for nitrogen (N) and essential amino acids by increasing intake of a low-protein diet;
- The decrease in intake of a high-protein diet associated with different processes, including the high satiating effect of protein. Increasing the protein content per se in the diet usually reduces energy intake and fat deposition in animal models.
There is a significant inverse relationship between protein content and energy intake, either in the context of a low or high fat diet. A high-protein diet also seems to induce sustained reductions in appetite, and libitum caloric intake, and body weight in humans.
The reduction of food intake induced by protein is due to a specific and independent effect of the protein content of the diet on satiety. Ingested proteins are believed to generate pre- and postabsorptive signals that contribute to the control of food intake.
Firstly, amino acid and oligopeptides are detected in the the intestine, the portal vein and/or the liver by specific amino acid and oligopeptides sensor systems. This information is for the main part transferred through the vagus nerve that innervates part of the oro-sensory zone.
At the brain level, two major afferent pathways are involved in protein and amino acid monitoring: the indirect neuro-mediated (mainly vagus-mediated) pathway recording visceral (gut, liver) informations and the direct monitoring of amino acids level and profile in the peripheral blood.
Three main CNS areas have been involved in the detection of amino acids: the brainstem (AP, NTS), the hypothalamus (AN, LHA), and the anterior pyriform cortex. It is likely that the indirect vagus-mediated pathway is involved in the control of meal intake whereas the direct blood pathway is involved in the control of blood amino acid disproportions.
Q. Can you comment on whether taste or palatability is a factor when you increase the protein content of the diet?
A. There are some data that taste or palatability can affect short-term food intake, but not long-term.
Q. Do you think that there is some metabolic signal responsible for making the animal prefer protein?
A. This might be the case, even if the palatability of the diet remains rather low.
Q. Is it the protein content of the diet or the % of protein in the diet?
A. It’s always problem to try to answer this question. If you increase one macronutrient, you will have to lower another. However, the effect of protein on satiety seems to be specific, and not related to the percentage in the diet.
Q. In all of these experiments, do you keep the fat content of the diet constant?
A. Yes, it’s always 10%.
Q. The animals that you use are young growing animals. Would you expect to get the same results if you were to use older animals?
A. We did get the same effect when we used older animals.
Q. So these data, the experiments comparing the P14 diet to the P50 diet, don’t suggest that protein enhances energy expenditure?
A. Right, that’s correct.
Q. What do you mean by “conditioned with palatability?”
A. After the first day, the animals decrease intake, but this effect goes away after a certain amount of time. Animals become conditioned to the palatability of the diet.
Q. Does the food intake increase due to the animals taking in smaller meals?
A. After the adaptation period or conditioning, the meal number decreases, but not meal size or duration.
Q. What kind of protein are you using in your diets?
A. Milk protein.
Q. Were the animals ketonic on the 0% carbohydrate diet?
Q. So that plays into energy reduction, the animals being in ketosis?
A. Yes, but both groups were in ketosis, so it should not affect the results.
Q. In the ad libitum diet, were animals choosing among foods that were high in protein?
A. Yes, that’s correct.
Q. How do you know that proteins stimulate afferent nerve fibers when infused into the duodenum?
A. That’s true, it could be a reflex response.
Q. In your diagram, what is PEPT1?
A. The reentry peptide transport system in the intestinal lumen.
Q. Has anyone looked at the effect of APC lesions on protein self-selection?
A. We did some lesions in animals, and animals still recognized and selected high protein diets.
Q. How long can animals survive on an amino acid deficient diet?
A. A couple of weeks, but then they die of starvation.
Q. Has anyone tried to do both a vagotomy and use a CCK antagonist and then look at food intake in rats?
A. No, not that I’m aware of.
Q. Is it possible that high protein diets really reduce the body set point or settling point?
A. Well, I agree that animals do find adaptation with a lower level of body fat when consuming high-protein diets.
Q. What do you mean by “short-term?”
A. Short-term refers to a meal.
Q. Why do your animals self-select a 50% protein diet?
A. I think this is due to a metabolic signal that has to do with glucose or insulin homeostasis.
Q. Did you say that when you lesion the APC, it does not decrease food intake?
A. Yes, that is correct.
Q. Have you looked at the effect of capsaicin?
A. We just did, and the capsaicin enhanced the suppression of protein on food intake.