Nutritional programming of insulin resistance: causes and consequences

Duque-Guimarães, Daniella E.; Ozanne, Susan E.

doi:10.1016/j.tem.2013.05.006

Cited by 123 publications

(92 citation statements)

References 146 publications

(150 reference statements)

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“…In any event, be it prenatally or postnatally, a high carbohydrate supply has been associated with alterations in insulin secretion, insulin resistance and impaired glucose metabolism often characterised by higher gluconeogenic output in adult mammals (Patel and Srinivasan, 2002;Patel et al, 2009). Analogous observations have been made in offspring following maternal protein restriction or intrauterine growth retardation, displaying glucose intolerance (Frantz et al, 2012;Duque-Guimarães and Ozanne, 2013;Kongsted et al, 2014), increased hepatic glucose output, reduced glucose phosphorylation (Desai et al, 1995;Ozanne et al, 1996) and altered glucose uptake by muscle skeletal cells as reflected by reduced Glut4 expression (Thamotharan et al, 2005;Devaskar and Thamotharan, 2007). In mammals, these are common signs of defects in glucose metabolism related to insulin resistance (AbdulGhani and DeFronzo, 2010).…”

mentioning

confidence: 68%

“…Prenatal or early nutritional neonatal events exerted during critical developmental windows may result in permanent changes in postnatal growth potential, health and metabolic status in mammals (Burdge and Lillycrop, 2010;Lucas, 1998;Patel and Srinivasan, 2002;Patel et al, 2009;Metges et al, 2014;Duque-Guimarães and Ozanne, 2013;Devaskar and Thamotharan, 2007). It has been RESEARCH ARTICLE 1 INRA, UR1067 Nutrition Metabolism and Aquaculture, F-64310 Saint-Pée-surNivelle, France.…”

Section: Introductionmentioning

confidence: 99%

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High or low dietary carbohydrate:protein ratios during first-feeding affect glucose metabolism and intestinal microbiota in juvenile rainbow trout

Geurden

Mennigen

Plagnes-Juan

et al. 2014

Journal of Experimental Biology

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Based on the concept of nutritional programming in mammals, we tested whether an acute hyperglucidic-hypoproteic stimulus during first feeding could induce long-term changes in nutrient metabolism in rainbow trout. Trout alevins received during the five first days of exogenous feeding either a hyperglucidic (40% gelatinized starch + 20% glucose) and hypoproteic (20%) diet (VLP diet) or a high-protein (60%) glucose-free diet (HP diet, control). Following a common 105-day period on a commercial diet, both groups were then challenged (65 days) with a carbohydrate-rich diet (28%). Short-and long-term effects of the early stimuli were evaluated in terms of metabolic marker gene expressions and intestinal microbiota as initial gut colonisation is essential for regulating the development of the digestive system. In whole alevins (short term), diet VLP relative to HP rapidly increased gene expressions of glycolytic enzymes, while those involved in gluconeogenesis and amino acid catabolism decreased. However, none of these genes showed persistent molecular adaptation in the liver of challenged juveniles (long term). By contrast, muscle of challenged juveniles subjected previously to the VLP stimulus displayed downregulated expression of markers of glycolysis and glucose transport (not seen in the short term). These fish also had higher plasma glucose (9 h postprandial), suggesting impaired glucose homeostasis induced by the early stimulus. The early stimulus did not modify the expression of the analysed metabolism-related microRNAs, but had short-and long-term effects on intestinal fungi (not bacteria) profiles. In summary, our data show that a short hyperglucidic-hypoproteic stimulus during early life may have a long-term influence on muscle glucose metabolism and intestinal microbiota in trout. KEY WORDS: Nutritional programming, Rainbow trout, Carbohydrates, Protein, Metabolism INTRODUCTIONPrenatal or early nutritional neonatal events exerted during critical developmental windows may result in permanent changes in postnatal growth potential, health and metabolic status in mammals (Burdge and Lillycrop, 2010;Lucas, 1998;Patel and Srinivasan, 2002;Patel et al., 2009;Metges et al., 2014;Duque-Guimarães and Ozanne, 2013;Devaskar and Thamotharan, 2007). It has been RESEARCH ARTICLE 1 INRA, UR1067 Nutrition Metabolism and Aquaculture, F-64310 Saint-Pée-surNivelle, France. suggested that this process of developmental plasticity utilizes the early nutritional cues to prepare individual phenotypes to better match the predicted future nutritional environment (Gluckman et al., 2005). Possible biological mechanisms for 'imprinting' the nutritional event until adulthood in mammalian vertebrates comprise adaptive changes in gene expression pattern or cellular phenotype (epigenetic phenomenon), nutrient-sensitive signalling pathways and adaptive clonal selection, which may be transmitted to future offspring (Lucas, 1998;Symonds et al., 2009;Waterland and Jirtle, 2003;Gut and Verdin, 2013). Experimental data on the concept...

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mentioning

confidence: 68%

Section: Introductionmentioning

confidence: 99%

High or low dietary carbohydrate:protein ratios during first-feeding affect glucose metabolism and intestinal microbiota in juvenile rainbow trout

Geurden

Mennigen

Plagnes-Juan

et al. 2014

Journal of Experimental Biology

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“…In the aggregate, in-depth studies have established that adverse pre- and postnatal environments have significant long-term effects on the risk of insulin resistance later in life [3]. The importance of healthy dietary choices is highlighted by the worrying trends for childhood obesity, which can be improved not only through improving the lifestyle of the children but also that of the parents.…”

Section: Discussionmentioning

confidence: 99%

“…It has been known for some time that dietary factors can influence the risk of insulin resistance, and in recent years it has come to light that this risk can be transmitted to offspring through intrauterine reprogramming events. Additionally, nutrition during early life has been shown to influence the development of metabolic diseases later in life [3]. Currently, management of type 2 diabetes (T2D) entails lifestyle changes, use of oral hypoglycemic agents, and injectable insulin.…”

Section: Introductionmentioning

confidence: 99%

In utero Exposure to Germinated Brown Rice and Its GABA Extract Attenuates High-Fat-Diet-Induced Insulin Resistance in Rat Offspring

Adamu

Imam²,

Ooi³

et al. 2017

Lifestyle Genomics

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Background: Numerous studies have reported on the influence of diet on insulin resistance. Our study provides insight into the effect of germinated brown rice (GBR) and γ-aminobutyric acid (GABA) on early environment-driven programming and susceptibility to insulin resistance in rat offspring. Methods: Male rat offspring from female Sprague-Dawley rats fed with a high-fat diet (HFD) alone, HFD + GBR, or HFD + GABA extract throughout pregnancy and lactation were weaned 4 weeks after delivery and followed up for 8 weeks. A biochemical analysis and an assessment of the hepatic expression of insulin signaling genes were performed. Results: The results showed that intrauterine exposure to HFD caused metabolic perturbations in rat offspring which gravitated towards insulin resistance even though the rat offspring did not consume an HFD. GBR and GABA attenuated the HFD-induced changes by underlying regulation of the insulin signaling genes. Conclusions: The results suggest that intake of GBR and GABA during pregnancy and lactation can influence the programming of genes in rat offspring, thereby enhancing insulin sensitivity.

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“…Several lines of evidence in both human and rodent studies support the concept that nutritional status during early development, including embryonic and fetal as well as early postnatal periods, programs metabolism and propensity to gain weight later in life (13)(14)(15)(16)(17)(18)(19). For example, in a historical cohort study, exposure to the Dutch famine of 1944-1945 during the fi rst half of pregnancy is associated with increased obesity rates in early adulthood, while exposure during the last trimester and the fi rst months of life is associated with reduced obesity rates ( 20 ).…”

Section: Real-time Quantitative Pcr Analysismentioning

confidence: 96%

Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance

Banh¹,

Nelson²,

Gao

et al. 2015

Journal of Lipid Research

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ids and metabolic energy. TAG synthesis in most cells starts with acylation of glycerol-3-phosphate, followed by two additional acylation steps, whereas in some cells it uses monoacylglycerol (MAG) as the initial acyl acceptor. AcylCoA:monoacylglycerol acyltransferase (MGAT) catalyzes the latter pathway and generates diacylglycerol for the fi nal acylation step ( 1 ). As MAG is mostly a degradation product of TAG, the MGAT pathway is thought to be important for recycling of TAG. Indeed, the best-characterized MGAT function is in the absorption of dietary fat. During the process, dietary TAG is hydrolyzed in the intestinal lumen to MAG and fatty acids. After uptake, the hydrolysis products are resynthesized to TAG in enterocytes for the assembly of chylomicron, which in turn delivers dietary lipids to peripheral tissues ( 2 ).Among three identifi ed genes encoding MGAT enzymes, Mogat2 is highly expressed in the intestine of both rodents and humans ( 3-6 ). Supporting the role of MGAT2 as an intestinal MGAT mediating fat absorption, constitutive global inactivation of the enzyme, through germ-line transmission of a null mutation in Mogat2 , greatly reduces intestinal MGAT activity and delays fat absorption ( 7 ). Interestingly, these Mogat2 Ϫ / Ϫ mice absorb a normal quantity of fat but are protected from obesity and other metabolic disorders induced by high-fat feeding. The underlying physiological mechanisms involve a transient decrease in food intake and a persistent increase in energy expenditure ( 7,8 ). Unexpectedly, the increase in energy expenditure does not require high-fat feeding, and MGAT2 defi ciency also protects Agouti mice from excess weight gain ( 9 ). Findings from both gain-and loss-of-function mouse models indicate that MGAT2 in the intestine is a major contributor but incompletely accounts for the Abstract Acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2 catalyzes triacylglycerol (TAG) synthesis, required in intestinal fat absorption. We previously demonstrated that mice without a functional MGAT2-coding gene ( Mogat2) exhibit increased energy expenditure and resistance to obesity induced by excess calories. One critical question raised is whether lacking MGAT2 during early development is required for the metabolic phenotypes in adult mice. In this study, we found that Mogat2 ؊ / ؊ pups grew slower than wildtype littermates during the suckling period. To determine whether inactivating MGAT2 in adult mice is suffi cient to confer resistance to diet-induced obesity, we generated mice with an inducible Mogat2 -inactivating mutation. Mice with adult-onset MGAT2 defi ciency ( Mogat2 AKO ) exhibited a transient decrease in food intake like Mogat2 ؊ / ؊ mice when fed a high-fat diet and a moderate increase in energy expenditure after acclimatization. They gained less weight than littermate controls, but the difference was smaller than that between wild-type and Mogat2 ؊ / ؊ mice. The moderate reduction in weight gain was associated with reduced hepatic TAG and improved glucose tolerance. Similar pr...

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Nutritional programming of insulin resistance: causes and consequences

Cited by 123 publications

References 146 publications

High or low dietary carbohydrate:protein ratios during first-feeding affect glucose metabolism and intestinal microbiota in juvenile rainbow trout

High or low dietary carbohydrate:protein ratios during first-feeding affect glucose metabolism and intestinal microbiota in juvenile rainbow trout

In utero Exposure to Germinated Brown Rice and Its GABA Extract Attenuates High-Fat-Diet-Induced Insulin Resistance in Rat Offspring

Adult-onset deficiency of acyl CoA:monoacylglycerol acyltransferase 2 protects mice from diet-induced obesity and glucose intolerance

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