ScienceDaily (Sep. 6, 2006) — The amount of a hunger-fighting hormone can be increased by eating a higher protein diet, researchers report in the September issue of the journal Cell Metabolism, published by Cell Press. The hormone, known as peptide YY (PYY), was earlier found by the researchers to reduce food intake by a third in both normal-weight and obese people when given by injection.
"We've now found that increasing the protein content of the diet augments the body's own PYY, helping to reduce hunger and aid weight loss," said Medical Research Council clinician scientist Rachel Batterham of University College London, who led the new study.
Scientists have known that high-protein content meals make people feel more full and reduce food intake, resulting in improvements in weight loss and weight loss maintenance. However, the mechanism responsible remained elusive.
In a study in normal-weight and obese people, the researchers now show that enhanced-protein meals stimulate greater release of PYY than either high-fat or high-carbohydrate meals and result in a greater reduction of hunger.
Further investigation in mice supported the human study results. High-protein diets reduced the number of calories animals consumed and increased their PYY levels. Mice fed a high-protein diet also gained less weight and produced more PYY than animals that ate the usual amount of protein, they found.
In addition, the researchers found that genetically modified mice unable to produce PYY ate more and became markedly obese. The genetically modified mice were also resistant to the beneficial effects of a high-protein diet, the researchers reported, demonstrating a direct connection between protein and PYY.
When the researchers treated those hormone-deficient mice with PYY, the animals lost weight.
"The findings show that PYY deficiency can cause obesity and that PYY appears to mediate the beneficial effects of increased-protein content diets," Batterham said. "One potential weight loss strategy is therefore to increase the satiating power of the diet and promote weight loss through the addition of dietary protein--harnessing our own satiety system.
"Such a diet is perhaps more typical to that of our hunter-gatherer ancestors," she added.
The average Western diet derives 49% of energy intake from carbohydrate, 35% from fat, and 16% from protein, Batterham said. That differs considerably from the diet of hunter-gatherers, who ate as much as twice the amount of protein.
Batterham cautioned, however, that large, long-term clinical trials are required before any particular diet could be recommended. She also noted that such a diet would not resemble the popular Atkins diet, which is typically high in both saturated fat and protein.
The researchers include Rachel L. Batterham, Helen Heffron, Saloni Kapoor, Joanna E. Chivers, Keval Chandarana, and Dominic J. Withers of the University College London in London, UK; Carel W. Le Roux of Hammersmith Hospital, Imperial College in London, UK; . Louise Thomas and Jimmy D. Bell of Imperial College London, Hammersmith Hospital Campus in London, UK; Herbert Herzog of The Garvan Institute of Medical Research, St. Vincent's Hospital in Sydney, Australia.
This work was supported by grants from the Medical Research Council (R.L.B., D.J.W., J.E.C., and J.D.B.), Wellcome Trust (D.J.W.), UCLH Charities CDRC (R.L.B.), and Travers Legacy (R.L.B.) and grant no. 188 827 from the National Health and Medical Research Council of Australia (H.H.). R.L.B. is an MRC Clinician Scientist.
Adapted from materials provided by Cell Press, via EurekAlert!, a service of AAAS.
"We've now found that increasing the protein content of the diet augments the body's own PYY, helping to reduce hunger and aid weight loss," said Medical Research Council clinician scientist Rachel Batterham of University College London, who led the new study.
Scientists have known that high-protein content meals make people feel more full and reduce food intake, resulting in improvements in weight loss and weight loss maintenance. However, the mechanism responsible remained elusive.
In a study in normal-weight and obese people, the researchers now show that enhanced-protein meals stimulate greater release of PYY than either high-fat or high-carbohydrate meals and result in a greater reduction of hunger.
Further investigation in mice supported the human study results. High-protein diets reduced the number of calories animals consumed and increased their PYY levels. Mice fed a high-protein diet also gained less weight and produced more PYY than animals that ate the usual amount of protein, they found.
In addition, the researchers found that genetically modified mice unable to produce PYY ate more and became markedly obese. The genetically modified mice were also resistant to the beneficial effects of a high-protein diet, the researchers reported, demonstrating a direct connection between protein and PYY.
When the researchers treated those hormone-deficient mice with PYY, the animals lost weight.
"The findings show that PYY deficiency can cause obesity and that PYY appears to mediate the beneficial effects of increased-protein content diets," Batterham said. "One potential weight loss strategy is therefore to increase the satiating power of the diet and promote weight loss through the addition of dietary protein--harnessing our own satiety system.
"Such a diet is perhaps more typical to that of our hunter-gatherer ancestors," she added.
The average Western diet derives 49% of energy intake from carbohydrate, 35% from fat, and 16% from protein, Batterham said. That differs considerably from the diet of hunter-gatherers, who ate as much as twice the amount of protein.
Batterham cautioned, however, that large, long-term clinical trials are required before any particular diet could be recommended. She also noted that such a diet would not resemble the popular Atkins diet, which is typically high in both saturated fat and protein.
The researchers include Rachel L. Batterham, Helen Heffron, Saloni Kapoor, Joanna E. Chivers, Keval Chandarana, and Dominic J. Withers of the University College London in London, UK; Carel W. Le Roux of Hammersmith Hospital, Imperial College in London, UK; . Louise Thomas and Jimmy D. Bell of Imperial College London, Hammersmith Hospital Campus in London, UK; Herbert Herzog of The Garvan Institute of Medical Research, St. Vincent's Hospital in Sydney, Australia.
This work was supported by grants from the Medical Research Council (R.L.B., D.J.W., J.E.C., and J.D.B.), Wellcome Trust (D.J.W.), UCLH Charities CDRC (R.L.B.), and Travers Legacy (R.L.B.) and grant no. 188 827 from the National Health and Medical Research Council of Australia (H.H.). R.L.B. is an MRC Clinician Scientist.
Adapted from materials provided by Cell Press, via EurekAlert!, a service of AAAS.
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