Programming of intermediary metabolism

Petry, Clive J.; Ozanne, Susan E.; Hales, C. N.

doi:10.1016/s0303-7207(01)00627-x

Cited by 76 publications

(56 citation statements)

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“…38,39 Despite such anomalies, the demonstration that the low protein diet favours the later development of obesity in rat has been rather elusive. Even after giving high-fat high-sucrose 'cafeteria' diet, the low protein progeny does not appear to become more obese than rats that were fed normally in utero.…”

Section: Animal Models For Programming Of Obesitymentioning

confidence: 99%

“…Even after giving high-fat high-sucrose 'cafeteria' diet, the low protein progeny does not appear to become more obese than rats that were fed normally in utero. 38,40 In mice however, offspring of dams fed a low protein diet during pregnancy and caught up during lactation by nursing by control dams gained more weight when given free access to a cafeteria diet. 41 Our recent results (unpublished data) underline the importance of an early catch-up growth after intrauterine nutrient shortage, since in these conditions, rats develop a higher obesity rate than controls, both after protein or calorie restriction, whereas they do not in the absence of rapid catch-up growth.…”

Section: Animal Models For Programming Of Obesitymentioning

confidence: 99%

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Programming of obesity and cardiovascular disease

2004

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BACKGROUND: There is evidence that malnutrition in early life induces a growth retardation leading, in adult life, to manifest components of the metabolic syndrome. However, the impact on obesity seems less clearly established. OBJECTIVE: To review the effects of foetal and postnatal malnutrition on the programming of obesity in the context of the metabolic syndrome, as well as the link between central obesity and cardiovascular diseases. METHODS: Included in the review were recent papers exploring the mechanisms linking maternal nutrition with impaired foetal growth and later obesity, cardiovascular disease, hypertension and diabetes in humans and animals. RESULTS: The programming of obesity during foetal and early postnatal life depends of the timing of maternal malnutrition as well as the postnatal environment. Obesity arises principally in offspring submitted to malnutrition during early stages of gestation and which presented early catch-up growth. The programming may involve the dysregulation of appetite control or the hormonal environment leading to a context favourable to obesity development (hypersecretion of corticosteroids, hyperinsulinaemia and hyperleptinaemia and anomalies in the IGF axis). Adipose tissue secretes actively several factors implicated in inflammation, blood pressure, coagulation and fibrinolysis. The programmed development of intra-abdominal obesity after early growth restriction may thus favour higher prevalence of hypertension and cardiovascular diseases. CONCLUSIONS: Abdominal obesity appears in malnourished offspring and is aggravated by early catch-up growth. Higher rates of intra-abdominal obesity observed after growth restriction may participate to hypertension and create atherothrombotic conditions leading to the development of cardiovascular diseases.

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Section: Animal Models For Programming Of Obesitymentioning

confidence: 99%

Section: Animal Models For Programming Of Obesitymentioning

confidence: 99%

Programming of obesity and cardiovascular disease

2004

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“…Moreover, we have recently shown that an intrauterine LP diet changed the gene expression pattern in fetal islets among which 10% were genes coding for mitochondrial proteins (47). Later in life, the net result of the early protein deficiency was a progressive loss of pancreatic islet function and development of insulin resistance in the adult with sex-specific time course (8,13,41).It is increasingly obvious that the programming is sex specific. Recent clinical and experimental evaluations of the fetal origins of obesity (20,33), insulin resistance (33), and vascular dysfunction showed a role of sex in the issue (5, 50, 52).…”

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confidence: 99%

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confidence: 99%

Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat

Theys

Bouckenooghe

Ahn

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Theys N, Bouckenooghe T, Ahn M-T, Remacle C, Reusens B. Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat. Am J Physiol Regul Integr Comp Physiol 297: R1516 -R1525, 2009. First published September 16, 2009; doi:10.1152/ajpregu.00280.2009.-Mitochondrial dysfunction may be a long-term consequence of a poor nutritional environment during early life. Our aim was to investigate whether a maternal low-protein (LP) diet may program mitochondrial dysfunction in islets of adult progeny before glucose intolerance ensues. To address this, pregnant Wistar rats were fed isocaloric diets containing either 20% protein (control) or 8% protein (LP diet) throughout gestation. From birth, offspring received the control diet. The mitochondrial function was analyzed in islets of 3-mo-old offspring. Related to their basal insulin release, cultured islets from both male and female LP offspring presented a lower response to glucose challenge and a blunted ATP production compared with control offspring. The expression of malate dehydrogenase as well as the subunit 6 of the ATP synthase encoded by mitochondrial genome (mtDNA) was lower in these islets, reducing the capacity of ATP production through the Krebs cycle and oxidative phosphorylation. However, mtDNA content was unchanged in LP islets compared with control. Several consequences of protein restriction during fetal life were more marked in male offspring. Only LP males showed an increased reactive oxygen species production associated with a higher expression of mitochondrial subunits of the electron transport chain NADH-ubiquinone oxireductase subunit 4L, an overexpression of peroxisome proliferator-activated receptor-␥ and uncoupling protein-2, and a strongly reduced beta-cell mass. In conclusion, mitochondrial function is clearly altered in islets from LP adult offspring in a sex-specific manner. That may provide a cellular explanation for the earlier development of glucose intolerance in male than in female offspring of dams fed an LP diet. developmental programming; malnutrition; metabolic syndrome; insulin secretion EPIDEMIOLOGICAL AND EXPERIMENTAL evidence shows a convincing relationship between a poor intrauterine nutritional environment and the subsequent development of metabolic disorders like insulin resistance, obesity, and cardiovascular disease in adulthood (11,12). The original concept of fetal programming of Type 2 diabetes mellitus (T2DM) was proposed by Hales et al. (12) who found in a cohort of adult men who had been smaller at birth that they were six times more prone to develop T2DM compared with individuals heavier at birth. These first epidemiological clues of programming have been largely replicated in many studies throughout the world (17, 27, 61). Currently, this concept is widely accepted, but the mechanistic basis is unclear.Recently, attention has focused on the involvement of mitochondria as putative targets linking physiological and molecular consequences of environmental disorders du...

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“…However, there is increasing evidence that early-life events can shape the trajectory of aging and influence longevity. Both undernutrition and overnutrition during pregnancy can profoundly alter adult metabolic phenotypes, risk of various chronic diseases (particularly cardiovascular disease and diabetes), and longevity (Barker et al 1993;Beauchamp et al 2015;Berends et al 2013;Blackmore and Ozanne 2013;Blackmore et al 2012;Petry et al 2001). In animals with genetic defects in endocrine function, hormonal replacement therapy during the early postnatal development period can alter longevity Panici et al 2010;Podlutsky et al 2017;Sonntag et al 2005;Tarantini et al 2016).…”

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confidence: 99%

Differential effects of early-life nutrient restriction in long-lived GHR-KO and normal mice

et al. 2017

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There is increasing evidence that growth hormone (GH) and insulin-like growth factor 1 (IGF-1) signaling (collectively referred to as somatotropic signaling) during development has a profound influence on aging and longevity. Moreover, the absence of GH action was shown to modify responses of adult mice to calorie restriction (CR) and other antiaging interventions. It was therefore of interest to determine whether GH resistance in GH receptor knockout (GHR-KO) mice would modify the effects of mild pre-weaning CR imposed by increasing the number of pups in a litter (the so-called litter crowding). In addition to the expected impact on body weight, litter crowding affected glucose homeostasis, hepatic expression of IGF-1 and genes related to lipid metabolism, and expression of inflammatory markers in white adipose tissue, with some of these effects persisting until the age of 2 years.Litter crowding failed to further extend the remarkable longevity of GHR-KO mice and, instead, reduced late life survival of GHR-KO females, an effect opposite to the changes detected in normal animals. We conclude that the absence of GH actions alters the responses to pre-weaning CR and prevents this intervention from extending longevity.

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Programming of intermediary metabolism

Cited by 76 publications

References 74 publications

Programming of obesity and cardiovascular disease

Programming of obesity and cardiovascular disease

Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat

Differential effects of early-life nutrient restriction in long-lived GHR-KO and normal mice

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