[PHNUTR-L] Why dieting mothers have fat kids

[jikeda]

>

>Public release date: 7-Jun-2005

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>Contact: Heidi Hardman

><mailto:hhardman at cell.com>hhardman at cell.com

>1-617-397-2879

><http://www.cellpress.com/>Cell Press

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>Link between mothers' poor diets, kids' obesity

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>New work may have found the missing link between mothers' diets and 

>obesity in kids. A study published in the June issue of Cell Metabolism 

>suggests that a hormone may explain the connection between mothers who are 

>poorly nourished and an increased risk of obesity in their children.

>

>The study reports evidence that a premature surge of the hormone leptin in 

>newborn mice of underfed mothers leads to a remodeling of key brain 

>circuits that contributes to obesity in the animals later in life. 

>Moreover, the researchers found that the early leptin surge alone was 

>enough to cause the accelerated weight gain.

>

>The findings offer one mechanism whereby metabolic disease can originate 

>from early developmental experiences, the researchers said.

>

>"Obesity has increased at an alarming rate in Western countries and is now 

>a worldwide public health problem," said Shingo Fujii of the Kyoto 

>University Graduate School of Medicine in Japan. "Genetic and 

>environmental factors, such as a high-calorie diet, are thought to 

>contribute to the prevalence of obesity.

>

>"The present study suggests that a premature surge of leptin as a result 

>of fetal undernourishment can alter energy regulation by the brain and 

>contribute to developmental origins of health and disease."

>

>Leptin is a hormone produced by fat that normally decreases food intake 

>and increases energy expenditure. In many species, including humans, the 

>hormone acts to stabilize weight and glucose balance through its effects 

>on leptin receptors in a portion of the brain called the hypothalamus.

>

>Earlier studies have found that mice lacking leptin show marked obesity 

>that is restored following leptin treatment. However, obese animals often 

>exhibit resistance to leptin's usual effects and high blood concentrations 

>of the hormone.

>

>Evidence has also suggested that a neonatal surge of leptin may play an 

>important role in the formation of energy-regulating brain circuits in the 

>hypothalamus.

>

>In the new study, mice born of mothers who ate 30 percent less than normal 

>were small at birth and had less fat. However, the undernourished newborns 

>caught up with normal mice after ten days and, when fed a high-fat diet, 

>developed pronounced weight gain and increased leptin levels compared to 

>normal mice on the same diet.

>

>The undernourished mice had lower body temperatures than normal mice, 

>suggesting that the prenatal nutritional deficiency "programmed" them to 

>conserve energy, the researchers said. During the catch-up growth period, 

>the transient rise in leptin levels normally seen in newborns occurred six 

>to eight days earlier in undernourished animals.

>

>When the researchers mimicked that premature leptin surge by administering 

>the hormone to normally fed mice, those animals also became prone to 

>obesity upon eating a diet high in fat.

>

>"Unexpectedly, normal offspring treated with leptin as newborns were 

>indistinguishable from those that were undernourished before birth," Fujii 

>said. "Premature onset of leptin surge is thus causally related to 

>pronounced obesity in undernourished offspring on a high-fat diet."

>

>The researchers further demonstrated that the mice experiencing a 

>premature surge of fat hormone exhibited resistance to administered 

>leptin, with impaired transport of the hormone to the brain and 

>abnormalities in the hypothalamic brain region that governs leptin 

>response. The findings suggest that the leptin surge may be a target for 

>therapeutic intervention in the developmental origins of health and 

>disease, the researchers said.

>

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>The researchers include Shigeo Yura, Hiroaki Itoh, Norimasa Sagawa, 

>Hiroaki Masuzaki, Kazuwa Nakao, Makoto Kawamura, Maki Takemura, Kazuyo 

>Kakui, and Shingo Fujii of Kyoto University Graduate School of Medicine; 

>Hiroshi Yamamoto of Shiga University of Medical Science; and Yoshihiro 

>Ogawa of Tokyo Medical and Dental University. This work was supported in 

>part by Grants-In-Aid for the Scientific Research from the Ministry of 

>Education, Science, and Culture, Japan and by grants from the Ministry of 

>Health and Welfare, the Smoking Research Foundation, the Mitsui Sumitomo 

>Insurance Welfare Foundation, Astellas Foundation for Research on 

>Metabolic Disorders, Ono Medical Research Foundation, and Daiwa Securities 

>Health Foundation.

>

>Yura, S., Itoh, H., Sagawa, N., Yamamoto, H., Masuzaki, H., Nakao, K., 

>Kawamura, M., Takemura, M., Kakui, K., Ogawa, Y., and Fujii, S. (2005). 

>Role of premature leptin surge in obesity resulting from intrauterine 

>undernutrition. Publishing in Cell Metabolism, June, 2005, Vol. 1, pages 

>371-378. DOI 10.1016/j.cmet.2005.05.005

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Joanne P. Ikeda, MA,RD
Cooperative Extension Nutrition Education Specialist & Lecturer
223 Morgan Hall
Nutritional Sciences Department
University of California
Berkeley, CA 94720-3104
phone (510)642-2790
FAX (510)642-4160
email: jikeda at berkeley.edu
^^^Please note this is a new email address.


See website of the Center for Weight and Health:  http://cnr.berkeley.edu/cwh 
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