Development of metabolic systems

Grove, Kevin L.; Grayson, Bernadette E.; Glavas, Maria M.; Xiao, Xiao Q.; Smith, M. Susan

doi:10.1016/j.physbeh.2005.08.063

Cited by 146 publications

(111 citation statements)

References 184 publications

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“…Although we did not measure food consumption in the offspring, other studies indicate that variable fat deposition may be due to differences in feeding behavior. 32 The hypothalamic pathways responsible for appetite regulation develop already in utero [39][40][41] and continue to develop during lactation in rats. 40,42 An alternative explanation for the susceptibility of male offspring to maternal LP diet may be that energy expenditure is reduced compared with females, either by reduced basal metabolic rate or lower activity levels.…”

Section: Discussionmentioning

confidence: 99%

Maternal preconceptional nutrition leads to variable fat deposition and gut dimensions of adult offspring mice (C57BL/6JBom)

et al. 2010

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Background: Maternal nutrition during pregnancy or lactation may affect the chance of offspring becoming obese as adults, but little is known regarding the possible role of maternal nutrition before conception. In this study, we investigate how variable protein and carbohydrate content of the diet consumed before pregnancy affects fat deposition and gut dimensions of offspring mice. Methods: Eight-week-old female mice (C57BL/6JBom) were fed isocaloric low protein (8.4% protein; LP), standard protein (21.5% protein; ST) or high protein (44.2% protein; HP) diets. After 8 weeks of feeding, females were mated and fed a standard laboratory chow diet (22.5% protein) throughout periods of mating, gestation, lactation and weaning. Offspring mice were fed the same standard diet up to 46 days of age. Then offspring were killed and measures of dissected fat deposits and of the digestive system were taken. Results: Fat deposition of the offspring was significantly affected by preconceptional maternal nutrition and the effects differed between sexes. Male offspring deposited most fat when mothers were fed the LP diet, whereas female offspring deposited most fat when mothers were fed the ST diet. The mass and length of the digestive organs were affected by preconceptional maternal nutrition. Total gut from pyloric sphincter to anus was significantly shorter and dry mass was heavier in mice whose mothers were fed LP diets compared with offspring of mothers fed ST diets or HP diets. There was no significant effect of maternal nutrition on dry mass of the stomach or ceca. Conclusion: Our study shows that preconceptional nutrition can have important influence on several body features of offspring in mice, including body composition and dimensions of the digestive system.

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Section: Discussionmentioning

confidence: 99%

Maternal preconceptional nutrition leads to variable fat deposition and gut dimensions of adult offspring mice (C57BL/6JBom)

et al. 2010

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“…The adipokine hormone leptin and the gut hormone ghrelin act on neural circuitry of the hypothalamus important for energy homeostasis and the regulation of the SNS. 4,5 We have recently shown that the renal sympathetic nerve activity (RSNA) and BP increases in the first few days of consuming a high-fat diet (HFD) in rabbits can be largely reversed by a leptin antagonist given intracerebroventricularly (ICV). [6][7][8][9] In contrast, ghrelin secreted by the stomach activates arcuate neurons containing neuropeptide Y and agouti-related protein and has been shown to suppress sympathetic activity, decrease BP, and stimulate appetite.…”

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confidence: 99%

Exposure to a High-Fat Diet During Development Alters Leptin and Ghrelin Sensitivity and Elevates Renal Sympathetic Nerve Activity and Arterial Pressure in Rabbits

et al. 2014

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With the rising prevalence of obesity, particularly among women of reproductive age, it is important to understand the consequences of maternal obesity and nutrient excess on processes underlying development because they may lead to adverse outcomes in offspring. Animal models of maternal fat-rich diets that reflect the dietary intakes of humans in affluent societies have demonstrated the programming of offspring hyperphagia, adiposity, insulin resistance, and hypertension.1,2 Various factors, including elevated blood pressure (BP), insulin resistance, hyperglycemia, elevated plasma glucocorticoids, and leptin, associated with obesity during gestation can affect the development of a fetus.3 These factors can all contribute to a suboptimal intrauterine environment and predispose offspring to an increased risk of obesity and hypertension. There is evidence that the sympathetic nervous system (SNS) may be activated in offspring of fat-fed dams that develop hypertension, 1 but to date no study has shown direct evidence for increased sympathetic vasomotor activity. The adipokine hormone leptin and the gut hormone ghrelin act on neural circuitry of the hypothalamus important for energy homeostasis and the regulation of the SNS. 4,5 We have recently shown that the renal sympathetic nerve activity (RSNA) and BP increases in the first few days of consuming a high-fat diet (HFD) in rabbits can be largely reversed by a leptin antagonist given intracerebroventricularly (ICV). [6][7][8][9] In contrast, ghrelin secreted by the stomach activates arcuate neurons containing neuropeptide Y and agouti-related protein and has been shown to suppress sympathetic activity, decrease BP, and stimulate appetite.10,11 Thus, both leptin and ghrelin may play a key role in the association between obesity and hypertension and may also be involved in the hypertension programmed by a maternal HFD (m-HFD).The purpose of this study was to examine the effect of an m-HFD during development on arterial pressure and RSNA and the central sympathetic effects of leptin and ghrelin in offspring. We used a rabbit model in which an HFD induces elevated BP and RSNA. [6][7][8][9] We hypothesized that offspring exposed to an HFD during development would retain greater deposits of fat and show a selective leptin-resistant phenotype Abstract-Exposure to maternal obesity or a maternal diet rich in fat during development may have adverse outcomes in offspring, such as the development of obesity and hypertension. The present study examined the effect of a maternal high-fat diet (m-HFD) on offspring blood pressure and renal sympathetic nerve activity, responses to stress, and sensitivity to central administration of leptin and ghrelin. Offspring of New Zealand white rabbits fed a 13% HFD were slightly heavier than offspring from mothers fed a 4% maternal normal fat diet (P<0.05) but had 64% greater fat pad mass (P=0.015). Mean arterial pressure, heart rate, and renal sympathetic nerve activity at 4 months of age were 7%, 7%, and 24% greater, respectively (P<0.001),...

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“…The neuronal metabolic systems in humans and primates develop prenatally, while in rodents these systems develop during the first 3 postnatal weeks (5,21). This results in the activation and optimization of neuronal systems during early rodent development.…”

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confidence: 99%

Pmchexpression during early development is critical for normal energy homeostasis

Mul

Berg³

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Mul JD, Yi CX, van den Berg SAA, Ruiter M, Toonen PW, van der Elst MCJ, Voshol PJ, Ellenbroek BA, Kalsbeek A, la Fleur SE, Cuppen E. Pmch expression during early development is critical for normal energy homeostasis. Am J Physiol Endocrinol Metab 298: E477-E488, 2010. First published November 24, 2009 doi:10.1152/ajpendo.00154.2009.-Postnatal development and puberty are times of strong physical maturation and require large quantities of energy. The hypothalamic neuropeptide melanin-concentrating hormone (MCH) regulates nutrient intake and energy homeostasis, but the underlying mechanisms are not completely understood. Here we use a novel rat knockout model in which the MCH precursor Pmch has been inactivated to study the effects of loss of MCH on energy regulation in more detail. Pmch Ϫ/Ϫ rats are lean, hypophagic, osteoporotic, and although endocrine parameters were changed in pmch Ϫ/Ϫ rats, endocrine dynamics were normal, indicating an adaptation to new homeostatic levels rather than disturbed metabolic mechanisms. Detailed body weight growth and feeding behavior analysis revealed that Pmch expression is particularly important during early rat development and puberty, i.e., the first 8 postnatal weeks. Loss of Pmch resulted in a 20% lower set point for body weight that was determined solely during this period and remained unchanged during adulthood. Although the final body weight is diet dependent, the Pmch-deficiency effect was similar for all diets tested in this study. Loss of Pmch affected energy expenditure in both young and adult rats, although these effects seem secondary to the observed hypophagia. Our findings show an important role for Pmch in energy homeostasis determination during early development and indicate that the MCH receptor 1 system is a plausible target for childhood obesity treatment, currently a major health issue in first world countries. melanin-concentrating hormone; hypothalamus; childhood obesity; rat knockout model CHILDHOOD OBESITY IS NOW WIDELY recognized as a severe public health issue (43). Treatment with drugs aimed at neural systems involved in the determination of the energy balance could potentially result in a lower energy balance during puberty as well as later in adulthood. Therefore, neuropeptides involved in body weight regulation during early development and puberty are attractive targets for anti-childhood obesity drugs.The neuronal metabolic systems in humans and primates develop prenatally, while in rodents these systems develop during the first 3 postnatal weeks (5, 21). This results in the activation and optimization of neuronal systems during early rodent development. A second important metabolic period is puberty, a period of major growth, hormonal changes, and sexual maturation. In the rat, puberty is characterized by different responses of young-adolescent [postnatal day (PND) 40] and young-adult (PND 60) male rats to environmental cues like stress and cold (17,18). In addition to these age-dependent behavioral differences, the amount of food consumed durin...

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Development of metabolic systems

Cited by 146 publications

References 184 publications

Maternal preconceptional nutrition leads to variable fat deposition and gut dimensions of adult offspring mice (C57BL/6JBom)

Maternal preconceptional nutrition leads to variable fat deposition and gut dimensions of adult offspring mice (C57BL/6JBom)

Exposure to a High-Fat Diet During Development Alters Leptin and Ghrelin Sensitivity and Elevates Renal Sympathetic Nerve Activity and Arterial Pressure in Rabbits

Pmchexpression during early development is critical for normal energy homeostasis

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