Lactation in lean and obese rats: Effect of cafeteria feeding and of dietary obesity on milk composition

Rolls, B. A.; Gurr, M. I.; Duijvenvoorde, P.M. Van; Rolls, Barbara J.; Rowe, Edward A.

doi:10.1016/0031-9384(86)90153-8

Cited by 84 publications

(74 citation statements)

References 18 publications

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“…Some studies in rodents have assessed influences of maternal high-energy diets using only a short time window, generally less than 14 days prior to mating or only during gestation and/or lactation, and have generally failed to achieve obesity in the dam [16,19,20,[24][25][26]. A few, using a prolonged feeding period to induce obesity [17,27,28], have generally switched from a high-energy diet to a control diet postdelivery [28], potentially inducing changes of the milk composition [29]. Since lactation may be a critical period for neonates in the programming of obesity, these protocols may affect the offspring phenotype [30].…”

Section: Discussionmentioning

confidence: 99%

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

et al. 2009

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Aims/hypothesis Accumulating evidence suggests that maternal obesity may increase the risk of metabolic disease in the offspring. We investigated the effects of established maternal diet-induced obesity on male and female offspring appetite, glucose homeostasis and body composition in rats. Methods Female Wistar rats were fed either a standard chow (3% fat, 7% sugar [wt/wt]) or a palatable obesogenic diet (11% fat, 43% sugar [wt/wt]) for 8 weeks before mating and throughout pregnancy and lactation. Male and female offspring of control and obese dams were weaned on to standard chow and assessed until 12 months of age. Results At mating, obese dams were heavier than control with associated hyperglycaemia and hyperinsulinaemia. Male and female offspring of obese dams were hyperphagic (p<0.0001) and heavier than control (p<0.0001) until 12 months of age. NEFA were raised at 2 months but not at 12 months. At 3 months, OGTT showed more pronounced alteration of glucose homeostasis in male than in female offspring of obese animals. Euglycaemic-hyperinsulinaemic clamps performed at 8 to 9 months in female and 10 to 11 months in male offspring revealed insulin resistance in male offspring of obese dams (p<0.05 compared with control). Body compositional analysis at 12 months also showed increased fat pad weights in male and female offspring of obese animals. Conclusions/interpretation Diet-induced obesity in female rats leads to a state of insulin resistance in male offspring, associated with development of obesity and increased adiposity. An increase in food intake may play a role.

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Section: Discussionmentioning

confidence: 99%

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

et al. 2009

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“…Consequently, it is important to understand the impact of maternal diet on the balance of specific fatty acids in the milk. However, while previous studies have reported that the total fat content of milk from mothers fed a cafeteria diet is significantly increased relative to those fed on standard rodent diets [12], there are currently no studies which have determined how these diets affect the fatty acid composition of the milk or the fatty acid status of the offspring.…”

Section: Introductionmentioning

confidence: 99%

Effect of a maternal cafeteria diet on the fatty acid composition of milk and offspring red blood cells

Vithayathil

Gugusheff

Gibson

et al. 2016

Prostaglandins, Leukotrienes and Essential Fatty Acids

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In all cases accepted manuscripts should:  link to the formal publication via its DOI  bear a CC-BY-NC-ND license -this is easy to do, click here to find out how  if aggregated with other manuscripts, for example in a repository or other site, be shared in alignment with our hosting policy  not be added to or enhanced in any way to appear more like, or to substitute for, the published journal article ABSTRACTPrevious studies have demonstrated that exposure to a maternal cafeteria diet during the lactation period alone produces detrimental effects to offspring metabolic health comparable to exposure during the entire perinatal period. The present study used a rodent model to assess the effect of a maternal cafeteria diet on the fat content and fatty acid composition of the dams' milk, and to determine the degree to which this was related to the fatty acid status of offspring on postnatal day 1 (PND1), weaning and 3 weeks post-weaning onto a standard rodent diet. As expected, omega-3 long chain polyunsaturated fatty acids (n-3 LCPUFA) content of both the milk and pup red blood cells (RBCs) was lower in the cafeteria (CAF) group on PND1. At 2 weeks post-partum, milk produced by CAF dams had a higher total fat, saturated fat and n-6 PUFA content, however these differences were modest in comparison with the differences in maternal intake between groups. Offspring suckled by CAF dams had a lower n-3 LCPUFA and n-6 PUFA status at weaning and higher trans fatty acid levels at both weaning and 6 weeks of age. These findings indicate that the fat content and fatty acid composition of the dam's milk is altered by exposure to a cafeteria diet. While it appears that the dam has a significant capacity to buffer the transfer of most dietary lipids into the milk, the trans fatty acids in particular appear to be readily transferred, resulting in persistent increases in trans fatty acid status of the offspring after weaning. The potential physiological implications of this warrants further explanation.

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“…These results demonstrate that postnatal factors can overcome both genetic predisposition and prenatal factors in determining the development of adiposity, insulin sensitivity, and the brain pathways that mediate these functions. diet-induced obesity; hypothalamus; milk; development; plasticity; Agouti-related peptide; leptin MATERNAL INTAKE of a high-fat diet and the presence of obesity during pregnancy and lactation promote obesity in offspring, particularly in individuals with an obesity-prone genetic background (21,32,36,55). However, there is growing evidence that a variety of manipulations during the postnatal environment can override prenatal factors and increase the risk of developing metabolic disorders such as obesity and diabetes later in life.…”

mentioning

confidence: 99%

“…MATERNAL INTAKE of a high-fat diet and the presence of obesity during pregnancy and lactation promote obesity in offspring, particularly in individuals with an obesity-prone genetic background (21,32,36,55). However, there is growing evidence that a variety of manipulations during the postnatal environment can override prenatal factors and increase the risk of developing metabolic disorders such as obesity and diabetes later in life.…”

mentioning

confidence: 99%

Postnatal environment overrides genetic and prenatal factors influencing offspring obesity and insulin resistance

Gorski

Dunn-Meynell²,

Hartman³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

191

205

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There is growing evidence that the postnatal environment can have a major impact on the development of obesity and insulin resistance in offspring. We postulated that cross-fostering obesity-prone offspring to lean, obesity-resistant dams would ameliorate their development of obesity and insulin resistance, while fostering lean offspring to genetically obese dams would lead them to develop obesity and insulin resistance as adults. We found that obesity-prone pups cross-fostered to obesity-resistant dams remained obese but did improve their insulin sensitivity as adults. In contrast, obesity-resistant pups cross-fostered to genetically obese dams showed a diet-induced increase in adiposity, reduced insulin sensitivity, and associated changes in hypothalamic neuropeptide, insulin, and leptin receptors, which might have contributed to their metabolic defects. There was a selective increase in insulin levels and differences in fatty acid composition of obese dam milk which might have contributed to the increased adiposity, insulin resistance, and hypothalamic changes in obesity-resistant cross-fostered offspring. These results demonstrate that postnatal factors can overcome both genetic predisposition and prenatal factors in determining the development of adiposity, insulin sensitivity, and the brain pathways that mediate these functions. diet-induced obesity; hypothalamus; milk; development; plasticity; Agouti-related peptide; leptin MATERNAL INTAKE of a high-fat diet and the presence of obesity during pregnancy and lactation promote obesity in offspring, particularly in individuals with an obesity-prone genetic background (21,32,36,55). However, there is growing evidence that a variety of manipulations during the postnatal environment can override prenatal factors and increase the risk of developing metabolic disorders such as obesity and diabetes later in life. Raising pups in small litters leads to increased milk intake and the development of obesity, whereas raising pups in large litters has the opposite effect (16,23,26). Administration of insulin during early postnatal development results in obesity and altered development of hypothalamic neuropeptide systems involved in energy homeostasis (22, 50). Cross-fostering pups is another method of assessing the role of the postnatal environment in later development. A single study in mice has demonstrated that fostering inbred obesity-prone mouse pups with obesity-resistant dams attenuates their obesity, whereas fostering obesity-resistant pups with obesity-prone dams causes them to develop obesity and insulin resistance (51).Unlike many rodent models, the majority of human obesity is inherited as a polygenic disorder (6). For that reason, we have used a rat model of diet-induced obesity (DIO), in which obesity is also inherited as a polygenic trait (33, 38) in association with insulin resistance (33), hypertension (14), and hyperlipidemia (62). These rats also have several abnormalities of brain function, which antedate and may contribute to the later development o...

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Lactation in lean and obese rats: Effect of cafeteria feeding and of dietary obesity on milk composition

Cited by 84 publications

References 18 publications

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

Effect of a maternal cafeteria diet on the fatty acid composition of milk and offspring red blood cells

Postnatal environment overrides genetic and prenatal factors influencing offspring obesity and insulin resistance

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