Maternal milk and plasma glucose and insulin levels: studies in normal and diabetic subjects.

Jovanovic‐Peterson, Lois; Fuhrmann, K; Hedden, K; Walker, Liberty; Peterson, Charles M.

doi:10.1080/07315724.1989.10720287

Cited by 80 publications

(64 citation statements)

References 14 publications

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“…Milk insulin levels were a good candidate, as insulin can cross the intestinal mucosa-blood barrier neonatally (18), and pups can absorb and assimilate large proteins like insulin from the maternal milk during the early postnatal period (24). Furthermore, insulin has neurotrophic properties in the developing brain (17,61,68).…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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

View full text Add to dashboard Cite

show abstract

“…There are also other possible explanations for childhood glucose intolerance and increased BMI in the offspring of PGDM mothers. Breast milk from women with type 1 diabetes has a higher glucose and energy content than breast milk from women without diabetes [36]. In some studies of the offspring of mothers with type 1 diabetes, the only variable that independently predicted offspring relative body weight at 2 years old was the volume of breast milk from the diabetic mother ingested during the first week of life, and the risk of childhood IGT was significantly lower in offspring fed banked breast milk from mothers without diabetes [37].…”

Section: Discussionmentioning

confidence: 99%

Absence of telomere shortening and oxidative DNA damage in the young adult offspring of women with pre-gestational type 1 diabetes

et al. 2008

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Aims/hypothesis The offspring of mothers with pre-gestational type 1 diabetes (PGDM) may be at increased risk of glucose intolerance and cardiovascular disease in childhood. The underlying causes of these observations, and whether they persist into adulthood, are unknown. The aim of the present study was to test the hypothesis that fetal chromosomal telomere oxidative DNA damage resulting from maternal PGDM programmes the offspring towards a senescent phenotype that is detectable in young adulthood. Methods We studied 21 young adult offspring (age 16-23 years) with a maternal history of PGDM and 23 age-and weight-matched controls with no maternal history of diabetes. All participants underwent anthropometric assessments, a standard 75 g OGTT, measurement of peripheral blood mononuclear cell and skin fibroblast telomere length, fibroblast senescence, cell DNA damage (by determination of 8-oxoguanine levels using flow cytometry), plasma lipoprotein profiles (determined by nuclear magnetic resonance) and plasma levels of soluble adhesion molecules and inflammatory markers. ResultsThe groups did not differ significantly with respect to anthropometric measures, glucose tolerance, fasting and 2 h plasma insulin levels during OGTT, estimated peripheral insulin resistance, peripheral blood mononuclear cell or fibroblast telomere length, DNA damage or senescence in vitro, plasma NMR lipoprotein profiles or levels of highsensitivity C-reactive protein. Plasma concentrations of soluble intercellular adhesion molecule 1 (sICAM-1; p< 0.05) and IL-6 (p=0.08) were higher in the PGDM offspring. Conclusions/interpretation Young adult offspring of mothers with PGDM do not differ in terms of glucose tolerance, DNA damage or telomere length from controls of the same weight and BMI. This does not preclude such abnormalities at an earlier age, but there is no evidence of telomere damage as a pre-programming mechanism in the young adults enrolled in this study.

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“…This is in agreement with the results of the only other study on breast-feeding in Type I diabetes where Plagemann et al (2002) found (in 118 infants) that early ingestion of breast milk of diabetic mothers increases the risk of becoming overweight. The reasons for such overweight may include higher glucose levels in breast milk and especially higher insulin levels in milk of women with diabetes (Butte et al, 1987;Jovanovic-Peterson et al, 1989;Neubauer, 1990;van Beusekom et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Effect of breast milk of diabetic mothers on bodyweight of the offspring in the first year of life

et al. 2004

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Objective: There is increasing evidence that in healthy populations, breast-fed infants are leaner than formula-fed infants. It is of interest to know the effects of breast-feeding on infant weight in case of maternal diabetes, given the high incidence of fetal macrosomia and risk of childhood obesity in this population. Design and Subjects: As part of a nation-wide study in the Netherlands on diabetes and pregnancy, 229 women with Type 1 diabetes were sent a questionnaire on weight and height of their infant, the type of nutrition given during the first 6 weeks of life, the duration of lactation and intercurrent diseases during the first year of life. Results and conclusion: Our data show no significant difference between breast-,formula-, and mixed-fed infants in weight and body mass index (BMI) at 1 y of age, which is not in accordance with the findings in nondiabetic populations. Sponsorship: Novo Nordisk Farma BV, Alphen aan de Rijn, the Netherlands and the Cornelis Visser Foundation.

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Maternal milk and plasma glucose and insulin levels: studies in normal and diabetic subjects.

Cited by 80 publications

References 14 publications

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

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

Absence of telomere shortening and oxidative DNA damage in the young adult offspring of women with pre-gestational type 1 diabetes

Effect of breast milk of diabetic mothers on bodyweight of the offspring in the first year of life

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