“A fat found in olive oil, nuts and avocados could help naturally curb weight gain,” the Daily Mail reported. It said that scientists have found that the fat - oleic acid - triggers a reaction in the body that staves off hunger pangs, telling the brain that the body is no longer hungry. The newspaper said the study, on rats, found that oleic acid is converted into a fatty lipid hormone in the body, and it is this that increases feelings of fullness. It said the discovery could lead to new anti-obesity drugs.
The newspaper report is based on preliminary research in animals. Although the study provides more detail on the processes linking fat intake with sensations of hunger, it did not look at how it could affect weight. There is a long way to go before research in this area might provide new dietary or drug treatments for obesity in humans. Nuts, avocados and olive oil are energy-dense foods, and therefore high in calories. At present there are no suggested methods to eat them to gain any sort of weight loss. Anyone considering experimenting on their own diet would be well advised to consider the total calorie intake as well as the specific food (nuts) and nutrient (fat) components.
This study was carried out by Dr Gary J. Schwartz from the Diabetes Research Center at the Albert Einstein College of Medicine of Yeshiva University in New York, with colleagues from Universities and Institutes in California and Italy. The research was supported by the National Institute of Health, the Skirball Institute, the New Work Obesity Research Center and the Italian Ministry of Research. The study was published in the peer-reviewed scientific journal, Cell Metabolism.
In this animal study, the researchers investigated the association between fat consumption and obesity. They used rats and mice to identify the chemical messengers within the body that signal or control the animals’ fat intake.
The researchers say that previous studies have shown that the act of eating can cause the lining of the small-intestine to produce a type of fat (lipid) messenger called oleoylethanolamide (OEA). When this chemical is given to animals as a drug, it reduces the number or frequency of meals that they take. This is known as a ‘satiety response’, and suggests that an animal is no longer hungry.
At a molecular level, when this response occurs, the chemical OEA binds with (instructs) receptors (peroxisome proliferator activated receptors-alpha [PPAR-α]), and these regulate the absorption, storage and use of dietary fat.
In this study, the researchers infused a lipid solution of oleic acid (a substance found in olive oil) into part of the small intestine of rats, and looked at whether it stimulated the release of OEA. These experiments were repeated with infused amino acid (the building blocks of protein) and sugar (carbohydrate) solutions to see if they had similar effects to OEA. In a separate part of the study, the researchers infused a molecule that was similar to oleic acid directly into the rats’ abdominal cavities to test whether oleic acid needed to be eaten to be converted to OEA. They also tested whether mutant mice, which lacked a specific protein in the intestinal wall (CD36) thought to be involved in the absorption of fatty acids such as oleic acid, would be more or less able to produce OEA.
The effect of the lipid infusions on feeding behaviour was then compared between normal mice and mutant mice lacking CD36 or PPAR-α. The effect on the feeding patterns of mice lacking PPAR-α was also compared to that of normal mice.
The researchers found that an infusion of oleic acid into the top part of the small intestine of the animals stimulated the release of OEA, whereas infusions of amino acids or sugars did not.
They demonstrated that OEA was produced from the oleic acid infused into the intestine and not converted from the oleic acid substitute that was infused into the abdominal cavity. They say this suggests that it must be eaten to have this effect. They also discovered that OEA was produced from oleic acid, but that this production was disrupted in mutant mice that lacked a specific protein in the intestinal wall (CD36).
Normal mice that were given the lipid infusion ate less, while mice that lacked either CD36 or PPAR-α did not eat less. Under normal conditions, mice lacking PPAR-α ate earlier and more often than normal mice, and this led to them eating more than normal mice over a 24-hour period. This suggested that the PPAR-α receptors normally act to delay the start of a subsequent meal, and that the disruption of the action of CD36 or of the PPAR-α receptors prevented this fat-induced satiety response.
The researchers say that the results suggest, “activation of small-intestinal OEA mobilisation, enabled by CD36-mediated uptake of dietary oleic acid, serves as a molecular sensor linking fat ingestion to satiety [the sensation of feeling full].”
They conclude that OEA is a key signal that specifically links dietary fat ingestion to satiety between meals. Strategies that amplified this signal, for example by inhibiting OEA degradation, might be useful in the treatment of obesity and other eating disorders.
This animal study has described and further clarified the role of a chemical messenger that is part of the complex pathway determining hunger and fat absorption in mice and rats. This is how new discoveries are made, some of which may in time translate into new treatments for human disease, while others further scientific knowledge without ever being directly applied to human medicine. It is too soon to say whether any proposed treatments from this study will be successful in humans.
Fats are essential in the diet, but are generally more energy-dense (contain more calories per unit weight) than other foods. As such, anyone considering experimenting on their own diet would be well advised to consider the total calorie intake as well as the specific food (nuts) and nutrient (fat) components. A well-balanced, nutritious diet and exercise remain the best advice for weight control and weight loss.