scholarly journals Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis

2006 ◽  
Vol 361 (1471) ◽  
pp. 1107-1121 ◽  
Author(s):  
Barry E Levin

Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre- versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the ‘metabolic syndrome’). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis.

2020 ◽  
Vol 11 (9) ◽  
pp. 7468-7480
Author(s):  
Peng Du ◽  
Junhan Zhou ◽  
Li Zhang ◽  
Jiaojiao Zhang ◽  
Nan Li ◽  
...  

Polyphenols extracted from Shanxi-aged vinegar (SAVEP) can alleviate oxidative stress and inflammatory stress caused by high-fat diets, improving intestinal microbial disorders. SAVEP may be a novel treatment of the metabolic syndrome.


Life Sciences ◽  
2016 ◽  
Vol 151 ◽  
pp. 70-75 ◽  
Author(s):  
Junya Ito ◽  
Kiyotaka Nakagawa ◽  
Shunji Kato ◽  
Taiki Miyazawa ◽  
Fumiko Kimura ◽  
...  

2005 ◽  
Vol 289 (1) ◽  
pp. R156-R163 ◽  
Author(s):  
C. Morens ◽  
M. Keijzer ◽  
K. de Vries ◽  
A. Scheurink ◽  
G. van Dijk

Changes in dietary macronutrient composition and/or central nervous system neuronal activity can underlie obesity and disturbed fuel homeostasis. We examined whether switching rats from a diet with high carbohydrate content (HC; i.e., regular chow) to diets with either high fat (HF) or high fat/high protein content at the expense of carbohydrates (LC-HF-HP) causes differential effects on body weight and glucose homeostasis that depend on the integrity of brain melanocortin (MC) signaling. In vehicle-treated rats, switching from HC to either HF or LC-HF-HP feeding caused similar reductions in food intake without alterations in body weight. A reduced caloric intake (−16% in HF and LC-HF-HP groups) required to maintain or increase body weight underlay these effects. Chronic third cerebroventricular infusion of the MC receptor antagonist SHU9119 (0.5 nmol/day) produced obesity and hyperphagia with an increased food efficiency again observed during HF (+19%) and LC-HF-HP (+33%) feeding. In this case, however, HF feeding exaggerated SHU9119-induced hyperphagia and weight gain relative to HC and LC-HF-HP feeding. Relative to vehicle-treated controls, SHU9119 treatment increased plasma insulin (2.8–4 fold), leptin (7.7–15 fold), and adiponectin levels (2.4–3.7 fold), but diet effects were only observed on plasma adiponectin (HC and LC-HF-HP<HF). Finally, SHU9119-treated LC-HF-HP-fed rats were less glucose tolerant than others. Relatively low plasma adiponectin levels likely contributed to this effect. Thus HF feeding amplifies obesity induced by impaired MC signaling, provided that the carbohydrate-to-protein (C/P) ratio is high enough. Reduction of the C/P ratio within a HF diet ameliorates hyperphagia and obesity in rats with impaired MC signaling but aggravates associated disturbances in fuel homeostasis.


2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Ting Luo ◽  
Sarah Smith ◽  
Bingxin Zhao ◽  
Jill Hamiton‐Reeves ◽  
Debra Sullivan ◽  
...  

2020 ◽  
Author(s):  
Yasmine J. Liu ◽  
Arwen W. Gao ◽  
Reuben L. Smith ◽  
Georges E. Janssens ◽  
Daan M. Panneman ◽  
...  

SUMMARYDeregulated energy homeostasis represents a hallmark of aging and results from complex gene-by-environment interactions. Here, we discovered that reducing the expression of the gene ech-6 encoding enoyl-CoA hydratase remitted fat diet-induced deleterious effects on lifespan in Caenorhabditis elegans, while a basal expression of ech-6 was important for survival under normal dietary conditions. Lipidomics revealed that supplementation of fat in ech-6-silenced worms had marginal effects on lipid profiles, suggesting an alternative fat utilization for energy production. Transcriptomics further suggest a causal relation between the lysosomal pathway, energy production, and the longevity effect conferred by the interaction between ech-6 and high-fat diets. Indeed, enhancing energy production from endogenous fat by overexpressing lysosomal lipase lipl-4 recapitulated the lifespan effects of high-fat diets on ech-6-silenced worms. Collectively, these results reveal that the gene ech-6 modulates metabolic flexibility and may be a target for promoting metabolic health and longevity.


2021 ◽  
Vol 8 ◽  
Author(s):  
Shenli Wang ◽  
Chongye Guo ◽  
Zhikai Xing ◽  
Meng Li ◽  
Haiying Yang ◽  
...  

White kidney beans contain α-amylase inhibitors that can be used in diet for weight reduction. In this study, we investigated the potential of white kidney bean (phaseolus vulgaris L.) extract enriched in α-amylase inhibitor as a food additive in yogurt to regulate blood glucose in hyperglycemic animals. Five groups of C57BL/6J mice were fed for 8 weeks with standard chow diets, high-fat diets (HFD), or high-fat diets with supplement of α-amylase inhibitor in white kidney beans (P. vulgaris extract, PVE), yogurt (Y), and PVE added yogurt (YPVE), respectively. The HFD weakened glucose tolerance and caused insulin resistance in mice, and changed the characteristics of intestinal flora. The intervention of Y, PVE, and YPVE decreased blood glucose, insulin, hyperlipidemia, and inflammatory cytokine levels in mice fed with HFD. Moreover, the YPVE could regulate the components of host intestinal microbiota toward a healthy pattern, significantly increased the metabolic-related flora Corynebacterium, Granulicatella, and Streptococcus, while it decreased Paraprevotella and Allobaculum. Thus, YPVE markedly increased functions of “Amino Acid Metabolism,” “Energy Metabolism,” “Nucleotide Metabolism,” and declined functions of “Glycan Biosynthesis and Metabolism.” Consequently, YPVE could be developed as a new functional food because of its beneficial prebiotic properties in the metabolic syndrome.


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