Improved Lactational Nutrition and Postnatal Growth Ameliorates Impairment of Glucose Tolerance by Uteroplacental Insufficiency in Male Rat Offspring

Siebel, Andrew L.; Mibus, Amy; Blasio, Miles J. De; Westcott, Kerryn T.; Morris, Margaret J.; Prior, Larissa J.; Owens, Julie A.; Wlodek, Mary E.

doi:10.1210/en.2008-0128

Cited by 71 publications

(152 citation statements)

References 43 publications

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“…Maternal caloric and protein restriction are the most widely used methods. In some studies, the growth of rat fetuses has been restricted by unilateral or bilateral uterine artery ligation in late gestation, which has led to impaired glucose tolerance in adult life (16). In addition, the effects of postnatal growth patterns vary between artery ligation studies, and there are also differences between the studies in the nutrition during lactation.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the effects of postnatal growth patterns vary between artery ligation studies, and there are also differences between the studies in the nutrition during lactation. Evidence for catch-up growth after lactation has (17,18) or has not been obtained (16). However, the majority of these studies have reported impaired glucose tolerance in male progeny by the time they reach adulthood (16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

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Plasma lipid levels and body weight altered by intrauterine growth restriction and postnatal fructose diet in adult rats

et al. 2012

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Background: Intrauterine growth restriction (IUGR) is known to affect the risk of adult diseases. consumption of lipogenic fructose is increasing, and it is used as an enhancer of metabolic syndrome in rat experiments. The effects of IUGR, postnatal fructose diet, and their interaction on the lipid profile and adiposity were studied in adult rats. Methods: IUGR was induced by providing pregnant rats with 50% of daily food intake. From 1 mo onward, half of the offspring received a fructose-rich diet and were then followed to the age of 1 and 6 mo, when plasma lipid, glucose, and insulin levels were measured. The adipose tissue was visualized by magnetic resonance imaging at the age of 6 mo. results: IUGR and fructose diet decreased body weight in adult rats. IUGR increased low-density lipoprotein cholesterol in 6-mo-old rats. The fructose diet evoked hypertriglyceridemia and hyperinsulinemia in both the sexes and decreased fasting glucose levels in female rats. Postnatal fructose diet increased lipid content percentage in the retroperitoneal and intra-abdominal adipose tissues in male rats. Interactions between IUGR and postnatal fructose diet were observed in adult weight in males. conclusion: These results demonstrate the importance of IUGR and fructose diet in adverse changes in lipid and glucose metabolism. t he terms "programming, " "fetal origins hypothesis, " and "metabolic imprinting" are used to describe the conditions in the uterus that can lead to possibly permanent or at least longterm changes in the systems involved in growth and metabolism (1,2). Epidemiological studies indicate that low birth weight is related to the risk of metabolic syndrome, type 2 diabetes, and atherosclerosis in adulthood. Poor fetal growth has also been linked to adult obesity, hypertension, and abnormal lipid metabolism (3).There is an interaction between the prenatal and postnatal environments on the health outcome of the offspring (3). Some, but not all, of the infants born small for gestational age show catch-up growth. Those experiencing early catch-up growth tend to have a higher BMI and fat mass as children (4), and according to some studies, they are at an increased risk for adult diseases as compared with those not showing catch-up growth (5). Therefore, it is interesting to elucidate the possible interactions between the prenatal growth and postnatal environment and their effects on the metabolic profile of the offspring.Fructose is a highly lipogenic sugar, and its consumption increases plasma triglyceride and low-density lipoprotein (LDL) cholesterol levels in humans (6). In rats, prolonged feeding of fructose induces moderate hypertension, glucose intolerance, insulin resistance, hyperinsulinemia, and hypertriglyceridemia, all of which are signs of metabolic syndrome (7,8). Therefore, fructose-fed rats are often used as a model of the metabolic syndrome (9).We performed a study of fetal growth restriction in rats. Initially, we aimed to determine if intrauterine growth restriction (IUGR) could affect plasma chole...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Plasma lipid levels and body weight altered by intrauterine growth restriction and postnatal fructose diet in adult rats

et al. 2012

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“…Since we have previously observed marked sex differences in a range of metabolic and cardiovascular outcomes in adult rats following uteroplacental insufficiency (20,29,31), it is possible there could be similar sex-specific effects on the expression of genes in the mitochondrial biogenesis pathway, GLUTs and antioxidant enzymes during cardiac development in growth restricted rats.…”

mentioning

confidence: 98%

“…Using well-established rodent models of uteroplacental insufficiency, our group, and others, have shown that growth restriction in prenatal and/or postnatal life adversely impacts on later metabolic and cardiovascular health in adulthood, including hypertension (27,31,32), cardiac hypertrophy (32), myocardial insulin resistance (26), impaired glucose tolerance (20), reduced cardiomyocyte number (5), and reduced expression of genes regulating mitochondrial biogenesis (synthesis) in skeletal muscle (29).…”

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confidence: 99%

Growth restriction in the rat alters expression of metabolic genes during postnatal cardiac development in a sex-specific manner

Wadley

McConell

Goodman

et al. 2013

Physiological Genomics

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“…Thus normalisation of the perinatal environment in the GK/ Par mother does not remove early BCM alteration and subsequent diabetes risk in the GK model. Early postnatal life is also important for the development and later function of beta cells, and it is clear that altered growth profiles in the postnatal period can affect adult metabolic homeostasis [28][29][30]. This is a matter of concern in the GK model, since we observed growth retardation during neonatal life in GK pups reared by GK mothers (nGK/sGK group) compared with W reared by non-diabetic W mothers (nW/sW group).…”

Section: Discussionmentioning

confidence: 84%

A euglycaemic/non-diabetic perinatal environment does not alleviate early beta cell maldevelopment and type 2 diabetes risk in the GK/Par rat model

Chavey¹,

Bailbé²,

Maulny³

et al. 2012

Diabetologia

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Aims/hypothesis We used the GK/Par rat, a spontaneous model of type 2 diabetes with early defective beta cell neogenesis, to determine whether the development of GK/Par offspring in a non-diabetic intrauterine/postnatal environment would prevent the alteration of fetal beta cell mass (BCM) and ultimately decrease the risk of diabetes later in adult life. Methods We used an embryo-transfer approach, with fertilised GK/Par ovocytes (oGK) being transferred into pregnant Wistar (W) or GK/Par females (pW and pGK). Offspring were phenotyped at fetal age E18.5 and at 10 weeks of age, for BCM, expression of genes of pancreatic progenitor cell regulators (Igf2, Igf1r, Sox9, Pdx1 and Ngn3), glucose tolerance and insulin secretion. Results (1) Alterations in neogenesis markers/regulators and BCM were as severe in the oGK/pW E18.5 fetuses as in the oGK/pGK group. (2) Adult offspring from oGK transfers into GK (oGK/pGK/sGK) had the expected diabetic phenotype compared with unmanipulated GK rats. (3) Adult offspring from oGK reared in pW mothers and milked by GK foster mothers had reduced BCM, basal hyperglycaemia, glucose intolerance and low insulin, to an extent similar to that of oGK/pGK/sGK offspring. (4) In adult offspring from oGK transferred into pW mothers and milked by their W mothers (oGK/pW/sW), the phenotype was similar to that in oGK/pGK/sGK or oGK/pW/sGK offspring. Conclusions/interpretation These data support the conclusion that early BCM alteration and subsequent diabetes risk in the GK/Par model are not removed despite normalisation of the prenatal and postnatal environments, either isolated or combined.

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Improved Lactational Nutrition and Postnatal Growth Ameliorates Impairment of Glucose Tolerance by Uteroplacental Insufficiency in Male Rat Offspring

Cited by 71 publications

References 43 publications

Plasma lipid levels and body weight altered by intrauterine growth restriction and postnatal fructose diet in adult rats

Plasma lipid levels and body weight altered by intrauterine growth restriction and postnatal fructose diet in adult rats

Growth restriction in the rat alters expression of metabolic genes during postnatal cardiac development in a sex-specific manner

A euglycaemic/non-diabetic perinatal environment does not alleviate early beta cell maldevelopment and type 2 diabetes risk in the GK/Par rat model

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