The effect of diet on food intake and adiposity in rats made obese by gestational undernutrition

Jones, Alan P.; Assimon, Sue Anne; Friedman, Mark I.

doi:10.1016/0031-9384(86)90194-0

Cited by 50 publications

(28 citation statements)

References 15 publications

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“…When rats are undernourished (50% decrease in energy intake) during the first 2 wk of pregnancy but refed during the third week, the male offspring develop significant hyperphagia and obesity when maintained on a high-fat diet (12,238,239,242). The obesity has a delayed onset (ϳ50 days of age) and is characterized by increases in the proportion of body fat and adipocyte hypertrophy in the epididymal and retroperitoneal fat pads.…”

Section: Programming Of Appetite: Ratmentioning

confidence: 99%

Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming

McMillen

Robinson²

2005

Physiological Reviews

1,689

1,352

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The "fetal" or "early" origins of adult disease hypothesis was originally put forward by David Barker and colleagues and stated that environmental factors, particularly nutrition, act in early life to program the risks for adverse health outcomes in adult life. This hypothesis has been supported by a worldwide series of epidemiological studies that have provided evidence for the association between the perturbation of the early nutritional environment and the major risk factors (hypertension, insulin resistance, and obesity) for cardiovascular disease, diabetes, and the metabolic syndrome in adult life. It is also clear from experimental studies that a range of molecular, cellular, metabolic, neuroendocrine, and physiological adaptations to changes in the early nutritional environment result in a permanent alteration of the developmental pattern of cellular proliferation and differentiation in key tissue and organ systems that result in pathological consequences in adult life. This review focuses on those experimental studies that have investigated the critical windows during which perturbations of the intrauterine environment have major effects, the nature of the epigenetic, structural, and functional adaptive responses which result in a permanent programming of cardiovascular and metabolic function, and the role of the interaction between the pre- and postnatal environment in determining final health outcomes.

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Section: Programming Of Appetite: Ratmentioning

confidence: 99%

Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming

McMillen

Robinson²

2005

Physiological Reviews

1,689

1,352

View full text Add to dashboard Cite

show abstract

“…It should be emphasized that those exposed to the Dutch Hunger Winter during late gestation (i.e., were born a few months into the famine) were also exposed during early infancy, whereas those exposed during early gestation (i.e., near the end of the famine) were born several months after the war when diets had improved. The importance of catch-up growth after adverse intrauterine conditions to the programming phenomenon has since been shown in numerous animal studies (10,11).…”

Section: Inappropriate Adaptationmentioning

confidence: 99%

The Dutch Hunger Winter and the developmental origins of health and disease

Schulz

2010

Proc. Natl. Acad. Sci. U.S.A.

372

220

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“…In the Dutch Hunger Winter Study, it was found that the offspring of women who were exposed to famine only during the first trimester of pregnancy grew up to have a higher body mass index, LDL/HDL ratio, and rate of cardiovascular disease than infants who developed before or after the famine [1] [2]. Similarly, offspring of sheep or rats that underwent nutrient restriction during early-mid pregnancy exhibited increased adiposity as adults [3] [4] [5]. Although deficiencies in individual dietary components such as methyl donors and protein have been implicated in this process, overall energy restriction likely plays a role [6] [7].…”

Section: Introductionmentioning

confidence: 99%

“…The effect of food restriction on serum leptin concentrations has not been examined during early pregnancy, a critical period for developmental programming [1,2,4,5]. During mid-pregnancy in sheep, nutrient restriction to 60% of metabolizable energy requirements (~40% ad libitum consumption) from days 28-80 resulted in significantly lower leptin concentrations than in pregnant controls [3].…”

Section: Introductionmentioning

confidence: 99%

The source of leptin, but not leptin depletion in response to food restriction, changes during early pregnancy in mice

Schlitt

Schulz

2011

Endocrine

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Maternal food restriction during pregnancy results in adverse consequences for offspring, including obesity and cardiovascular disease. Early pregnancy is a critical period for this programming effect. Leptin is a regulator of energy homeostasis that also affects placental and fetal development. As food restriction results in decreased serum leptin levels, at least in non-pregnant animals, leptin depletion may be one mechanism by which food restriction affects development. The goal of this study was to test whether moderate food restriction affects serum leptin concentrations during the first half of pregnancy. We found that restriction to 50% of ad libitum consumption levels resulted in a significant decrease in serum leptin concentrations in both pregnant and non-pregnant female mice. There was no significant difference in serum leptin concentrations between non-pregnant females and at pregnancy day 11.5 when fed ad libitum. However, there was a difference in the source of leptin during pregnancy, with greater production in visceral fat in pregnant mice, and greater production in subcutaneous fat in non-pregnant mice. Leptin concentrations were dependent on time of day and time of sampling relative to feeding, particularly in restricted mice. There was a significant difference in serum leptin concentrations between fed and restricted mice when they were fed and sampled in afternoon, but not when they were fed and sampled in morning. We conclude that food restriction results in a significant decrease in leptin concentration during the first half of pregnancy in mice, but that detection of this relationship is subject to experimental design considerations.

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The effect of diet on food intake and adiposity in rats made obese by gestational undernutrition

Cited by 50 publications

References 15 publications

Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming

Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming

The Dutch Hunger Winter and the developmental origins of health and disease

The source of leptin, but not leptin depletion in response to food restriction, changes during early pregnancy in mice

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