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Maternal obesity induced by diet in rats permanently influences central processes regulating food intake in offspring.

Kirk SL, Samuelsson AM, Argenton M, Dhonye H, Kalamatianos T, Poston L, Taylor PD, Coen CW - PLoS ONE (2009)

Bottom Line: Hypothalamic systems which regulate appetite may be permanently modified during early development.We have previously reported hyperphagia and increased adiposity in the adult offspring of rodents fed an obesogenic diet prior to and throughout pregnancy and lactation.At postnatal Day 30, before the onset of hyperphagia in these animals, serum leptin is normal, but leptin-induced appetite suppression and phosphorylation of STAT3 in the arcuate nucleus (ARC) are attenuated; the level of AgRP-immunoreactivity in the hypothalamic paraventricular nucleus (PVH), which derives from neurones in the ARC and is developmentally dependent on leptin, is also diminished.

View Article: PubMed Central - PubMed

Affiliation: Division of Reproduction and Endocrinology, King's College London, London, UK.

ABSTRACT
Hypothalamic systems which regulate appetite may be permanently modified during early development. We have previously reported hyperphagia and increased adiposity in the adult offspring of rodents fed an obesogenic diet prior to and throughout pregnancy and lactation. We now report that offspring of obese (OffOb) rats display an amplified and prolonged neonatal leptin surge, which is accompanied by elevated leptin mRNA expression in their abdominal white adipose tissue. At postnatal Day 30, before the onset of hyperphagia in these animals, serum leptin is normal, but leptin-induced appetite suppression and phosphorylation of STAT3 in the arcuate nucleus (ARC) are attenuated; the level of AgRP-immunoreactivity in the hypothalamic paraventricular nucleus (PVH), which derives from neurones in the ARC and is developmentally dependent on leptin, is also diminished. We hypothesise that prolonged release of abnormally high levels of leptin by neonatal OffOb rats leads to leptin resistance and permanently affects hypothalamic functions involving the ARC and PVH. Such effects may underlie the developmental programming of hyperphagia and obesity in these rats.

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Maternal body weight and food intake in rats fed control or obesogenic diet.Body weight (A) was recorded for 6 weeks prior to pregnancy and throughout pregnancy and lactation for the animals on the control (open symbols) or obesogenic (closed symbols) diet; calorific intake was recorded throughout pregnancy and lactation (B). Average daily calorific intake from all sources during pregnancy (C) and average daily calorific intake from fat or simple sugars during pregnancy (D) or lactation (E) for the animals on the control (Con) or obesogenic (Ob) diet. Macronutrient content of ingested food (expressed as percentage by weight) for control (F) or obese (G) dams during lactation; “other” includes cellulose, ash, water etc. * p<0.05 and ** p<0.01 versus control dams (n = 11–12).
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pone-0005870-g001: Maternal body weight and food intake in rats fed control or obesogenic diet.Body weight (A) was recorded for 6 weeks prior to pregnancy and throughout pregnancy and lactation for the animals on the control (open symbols) or obesogenic (closed symbols) diet; calorific intake was recorded throughout pregnancy and lactation (B). Average daily calorific intake from all sources during pregnancy (C) and average daily calorific intake from fat or simple sugars during pregnancy (D) or lactation (E) for the animals on the control (Con) or obesogenic (Ob) diet. Macronutrient content of ingested food (expressed as percentage by weight) for control (F) or obese (G) dams during lactation; “other” includes cellulose, ash, water etc. * p<0.05 and ** p<0.01 versus control dams (n = 11–12).

Mentions: Female Sprague Dawley rats consuming the highly palatable fat- and sugar-rich diet became significantly heavier than control animals after 10 days (Fig. 1A). After 6 weeks on this obesogenic diet, they were 20% heavier than controls, at which point they were mated. The weight difference was maintained throughout pregnancy by significantly increased calorific intake of both fat and simple sugars (Fig. 1A–D). During lactation, dams on the obesogenic diet continued to show a significantly higher calorific intake from fat and simple sugars than the control dams (Fig. 1E). The obese dams consumed approximately 4 times more fat and 5 times more simple sugars than the control dams during pregnancy and lactation (Fig. 1F,G; data presented for lactation; similar data for the pre-conditioning period and during pregnancy not shown).


Maternal obesity induced by diet in rats permanently influences central processes regulating food intake in offspring.

Kirk SL, Samuelsson AM, Argenton M, Dhonye H, Kalamatianos T, Poston L, Taylor PD, Coen CW - PLoS ONE (2009)

Maternal body weight and food intake in rats fed control or obesogenic diet.Body weight (A) was recorded for 6 weeks prior to pregnancy and throughout pregnancy and lactation for the animals on the control (open symbols) or obesogenic (closed symbols) diet; calorific intake was recorded throughout pregnancy and lactation (B). Average daily calorific intake from all sources during pregnancy (C) and average daily calorific intake from fat or simple sugars during pregnancy (D) or lactation (E) for the animals on the control (Con) or obesogenic (Ob) diet. Macronutrient content of ingested food (expressed as percentage by weight) for control (F) or obese (G) dams during lactation; “other” includes cellulose, ash, water etc. * p<0.05 and ** p<0.01 versus control dams (n = 11–12).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2690656&req=5

pone-0005870-g001: Maternal body weight and food intake in rats fed control or obesogenic diet.Body weight (A) was recorded for 6 weeks prior to pregnancy and throughout pregnancy and lactation for the animals on the control (open symbols) or obesogenic (closed symbols) diet; calorific intake was recorded throughout pregnancy and lactation (B). Average daily calorific intake from all sources during pregnancy (C) and average daily calorific intake from fat or simple sugars during pregnancy (D) or lactation (E) for the animals on the control (Con) or obesogenic (Ob) diet. Macronutrient content of ingested food (expressed as percentage by weight) for control (F) or obese (G) dams during lactation; “other” includes cellulose, ash, water etc. * p<0.05 and ** p<0.01 versus control dams (n = 11–12).
Mentions: Female Sprague Dawley rats consuming the highly palatable fat- and sugar-rich diet became significantly heavier than control animals after 10 days (Fig. 1A). After 6 weeks on this obesogenic diet, they were 20% heavier than controls, at which point they were mated. The weight difference was maintained throughout pregnancy by significantly increased calorific intake of both fat and simple sugars (Fig. 1A–D). During lactation, dams on the obesogenic diet continued to show a significantly higher calorific intake from fat and simple sugars than the control dams (Fig. 1E). The obese dams consumed approximately 4 times more fat and 5 times more simple sugars than the control dams during pregnancy and lactation (Fig. 1F,G; data presented for lactation; similar data for the pre-conditioning period and during pregnancy not shown).

Bottom Line: Hypothalamic systems which regulate appetite may be permanently modified during early development.We have previously reported hyperphagia and increased adiposity in the adult offspring of rodents fed an obesogenic diet prior to and throughout pregnancy and lactation.At postnatal Day 30, before the onset of hyperphagia in these animals, serum leptin is normal, but leptin-induced appetite suppression and phosphorylation of STAT3 in the arcuate nucleus (ARC) are attenuated; the level of AgRP-immunoreactivity in the hypothalamic paraventricular nucleus (PVH), which derives from neurones in the ARC and is developmentally dependent on leptin, is also diminished.

View Article: PubMed Central - PubMed

Affiliation: Division of Reproduction and Endocrinology, King's College London, London, UK.

ABSTRACT
Hypothalamic systems which regulate appetite may be permanently modified during early development. We have previously reported hyperphagia and increased adiposity in the adult offspring of rodents fed an obesogenic diet prior to and throughout pregnancy and lactation. We now report that offspring of obese (OffOb) rats display an amplified and prolonged neonatal leptin surge, which is accompanied by elevated leptin mRNA expression in their abdominal white adipose tissue. At postnatal Day 30, before the onset of hyperphagia in these animals, serum leptin is normal, but leptin-induced appetite suppression and phosphorylation of STAT3 in the arcuate nucleus (ARC) are attenuated; the level of AgRP-immunoreactivity in the hypothalamic paraventricular nucleus (PVH), which derives from neurones in the ARC and is developmentally dependent on leptin, is also diminished. We hypothesise that prolonged release of abnormally high levels of leptin by neonatal OffOb rats leads to leptin resistance and permanently affects hypothalamic functions involving the ARC and PVH. Such effects may underlie the developmental programming of hyperphagia and obesity in these rats.

Show MeSH
Related in: MedlinePlus