WELLINGTON, July 25 (Xinhua) -- New Zealand scientists have discovered new clues that help to explain why some people appear more likely than others to put on weight.

    Auckland's Liggins Institute released a report Wednesday suggesting that not all people are biologically the same.

    The study shows that the fetus takes cues from its life in the womb, such as the availability of nutrients, to predict what its future environment will be and chart a course of development that will fit it for that life.

    Thus, if a mother has a poor diet during pregnancy, her fetus might predict that future food supplies will be scarce and set its metabolism to store and conserve fat.

    However, if this early prediction proves false and food - particularly food high in fat - is readily available, the infant may find its metabolism programmed for adult obesity and conditions such as heart disease and diabetes.

    With colleagues at New Zealand's National Research Center for Growth and Development and The University of Southampton, the Liggins team led by Professor Peter Gluckman has been at the forefront of research linking the prenatal environment with long-term health outcomes.

    In a landmark study published two years ago the group provided the first experimental evidence that this developmental programming could be reversed.

    They dosed the newborn offspring of rats that had been undernourished during pregnancy, and were thus at risk of growing into obese adults, with the hormone leptin.

    Leptin is a naturally occurring hormone that regulates appetite and signals to the body when it has eaten enough. The pups that were treated with leptin went on to develop normally and did not become obese.

    In the latest study the scientists investigated the long-term effects of prenatal undernutrition followed by neonatal leptin treatment on key genes that regulate metabolism in the livers of adult rats.

    They found that the direction of the response to the second environmental signal, the leptin treatment, depended on the nature of the previous signal from the prenatal nutrient levels.

    In leptin-treated rats whose mothers had been well-fed, liver levels of an important protein that regulates stress hormone levels were much higher than normal.

    However, in treated rats whose mothers had been undernourished, the same protein was scarcer than normal.

    In this and several other measures of gene regulation, rats with well-fed mothers reacted to leptin in the opposite direction than did rats with undernourished mothers.

    "The study poses questions of fundamental importance that change the whole way we think about who we are," says Gluckman.

    The scientists raise the novel and exciting possibility that humans may have alternate forms, designed to be fat or thin, depending on nutritional signals received during fetal life.

    The results of their latest study will be published this week in the prestigious American journal Proceedings of the National Academy of Science.