Nutritional programming of disease: unravelling the mechanism

Langley‐Evans, Simon C.

doi:10.1111/j.1469-7580.2008.00977.x

Cited by 184 publications

(150 citation statements)

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“…A series of epidemiological, clinical and experimental studies performed throughout the world have demonstrated that there is an association among slow growth before birth; accelerated growth in early postnatal life; and the emergence of glucose intolerance, insulin resistance, type 2 diabetes and obesity in later life [26][27][28][29] . Our previous studies have found that the IUGR offspring with PNE who were fed a normal diet failed to present a significant "catch up" growth pattern of body weight [14] .…”

Section: Discussionmentioning

confidence: 99%

Prenatal nicotine exposure enhances the susceptibility to metabolic syndrome in adult offspring rats fed high-fat diet via alteration of HPA axis-associated neuroendocrine metabolic programming

Xia

Shen

et al. 2013

Acta Pharmacol Sin

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Aim: Prenatal nicotine exposure (PNE) alters the hypothalamic-pituitary-adrenocortical (HPA) axis-associated neuroendocrine metabolic programming in intrauterine growth retardation offspring rats. In this study we aimed to clarify the susceptibility to metabolic diseases of PNE offspring rats fed a high-fat diet. Methods: Maternal Wistar rats were injected with nicotine (1.0 mg/kg, sc) twice per day from gestational day 11 until full-term delivery, and all pups were fed a high-fat diet after weaning and exposed to unpredictable chronic stress (UCS) during postnatal weeks 18-20. Blood samples were collected before and after chronic stress, and serum ACTH, corticosterone, glucose, insulin, total cholesterol, triglyceride and free fatty acids levels were measured. The hypothalamus, pituitary gland and liver were dissected for histological studies. Results: UCS significantly increased the serum ACTH, corticosterone and insulin levels as well as the insulin resistant index without changing the serum glucose, total cholesterol, triglyceride and free fatty acids levels in adult offspring rats without PNE. The body weight of PNE offspring rats presented a typical "catch-up" growth pattern. PNE not only aggravated the UCS-induced changes in the HPA axis programmed alteration (caused further increases in the serum ACTH and corticosterone levels), but also significantly changed the glucose and lipid metabolism after UCS (caused further increases in the serum glucose level and insulin resistant index, and decrease in the serum free fatty acids). The effects of PNE on the above indexes after UCS showed gender differences. Pathological studies revealed that PNE led to plenty of lipid droplets in multiple organs. Conclusion: PNE enhances not only the HPA axis, but also the susceptibility to metabolic diseases in adult offspring rats fed a high-fat diet after UCS in a gender-specific manner and enhances the susceptibility to metabolic diseases in adult offspring rats fed a high-fat diet.

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Section: Discussionmentioning

confidence: 99%

Prenatal nicotine exposure enhances the susceptibility to metabolic syndrome in adult offspring rats fed high-fat diet via alteration of HPA axis-associated neuroendocrine metabolic programming

Xia

Shen

et al. 2013

Acta Pharmacol Sin

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“…The impact of the nutritional environment during early development is a wellestablished fact [370][371][372][373][374]. 5-HT could possibly have a twofold role here, as 5-HT synthesis depends on tryptophan of nutritional origin, but then the 5-HT satiety system controls feeding itself.…”

Section: Serotonin and The Pharmacotherapy Of Obesitymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

244

167

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Serotonin has been implicated in the control of satiety for almost four decades. Historically, the insight that the appetite suppressant effect of fenfluramine is linked to serotonin has stimulated interest in and research into the role of this neurotransmitter in satiety. Various rodent models, including transgenic models, have been developed to identify the involved 5-HT receptor subtypes. This approach also required the availability of receptor ligands of different selectivity, and behavioural techniques had to be developed simultaneously which allow differentiating between unspecific pharmacological effects of these ligands and 'true' 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 IntroductionWhat are the behavioural and physiological mechanisms that promote satiety? How is satiety defined? Satiety can be seen as a behavioural state which arises from food consumption and suppresses the initiation of eating for a particular period of time [1]. This description alone suggests a high degree of complexity as peripheral post-ingestive and post-absorptive signals need to be relayed to the brain where they are integrated with other signals to produce (or not) the behavioural state called satiety. The state of satiety is brought about a process called satiation, where sensory, cognitive and early post-ingestive mechanisms bring feeding to a halt and thus stopping a meal. Promoting satiation alone must not necessarily lead to reduced total food intake as the frequency of meals could be increased subsequently. Many peripheral and brain mechanisms have been identified that are involved in the expression satiety and it has been suggested that serotonin accelerates satiation and prolongs satiety [2]. In the following, we will review the role of serotonin in satiety in more detail 1 . The reader will see that, despite immense progress made during the last years, the field is still far from being resolved.As serotonin (5-Hydroxytryptamine; 5-HT) is a phylogenetically old neurotransmitter, various functions had time to evolve in different phyla, but maybe also in different species. 5-HT receptors exist in animal cells for millions of years and they are as old as adrenoreceptors ore some peptide receptors, possibly even older [5,6]. Even in invertebrates such as molluscs (Aplysia californica) and annelids (Hirudo medicinalis), 5-HT might functionally be related to food intake [7]. 5-HT is involved in feeding even in the honeybee where it has separate effects in the gut and in the insect brain [8]. In general, however, 5-HT seems rather to be involved in appetitive behaviours in invertebrates whereas it has more of a satiating effect in vertebrates [9]. In general, 5-HT neurons seem to be more extensively distributed throughout the body in lower animals than in higher animals including mammals where 5-HT neurones...

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“…This situation has led to increased violence, undernutrition and family breakdown, along with a reduction in the level of schooling. In addition, there is considerable evidence indicating that undernutrition in early life results in harmful consequences over the long term, including obesity, CVD and diabetes (7)(8)(9)(10) .…”

mentioning

confidence: 99%

A 15-year study on the treatment of undernourished children at a nutrition rehabilitation centre (CREN), Brazil

Fernandes

Lopez

Albuquerque

et al. 2011

Public Health Nutr.

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Objective: To build a life table and determine the factors related to the time of treatment of undernourished children at a nutrition rehabilitation centre (CREN), São Paulo, Brazil. Design: Nutritional status was assessed from weight-for-age, height-for-age and BMI-for-age Z-scores, while neuropsychomotor development was classified according to the milestones of childhood development. Life tables, Kaplan-Meier survival curves and Cox multiple regression models were employed in data analysis. Setting: CREN (Centre of Nutritional Recovery and Education), São Paulo, Brazil. Subjects: Undernourished children (n 228) from the southern slums of São Paulo who had received treatment at CREN under a day-hospital regime between the years 1994 and 2009. Results: The Kaplan-Meier curves of survival analysis showed statistically significant differences in the periods of treatment at CREN between children presenting different degrees of neuropsychomotor development (log-rank 5 6?621; P 5 0?037). Estimates based on the multivariate Cox model revealed that children aged $24 months at the time of admission exhibited a lower probability of nutritional rehabilitation (hazard ratio (HR) 5 0?49; P 5 0?046) at the end of the period compared with infants aged up 12 months. Children presenting slow development were better rehabilitated in comparison with those exhibiting adequate evolution (HR 5 4?48; P 5 0?023). No significant effects of sex, degree of undernutrition or birth weight on the probability of nutritional rehabilitation were found. Conclusions: Age and neuropsychomotor developmental status at the time of admission to CREN are critical factors in determining the duration of treatment.Undernutrition is characterised by a complex combination of factors including inadequate or insufficient ingestion of food, deficient intake of essential nutrients, unsatisfactory socio-economic conditions, unhealthy living environment, high frequency of infection and poor health care (1,2) . Evidently, the longer the exposure to such harmful factors the more damaging the consequences to the nutritional status of the individual. The height-for-age indicator reflects linear growth, and is related to long-term changes in nutritional status and overall health (3) . A deficit in this index is associated with cumulative growth retardation indicating chronic undernutrition. The problem of undernutrition is of global concern since, according to the latest FAO estimates, 925 million people ingest insufficient food to meet their minimum energy requirements, of whom 53 million live in Latin America and the Caribbean (4) . In developing countries, approximately 112 million children aged 5 years or less are affected by weight-for-age deficit and 32 % of children in this age group worldwide have been diagnosed with height-for-age deficit (2) . Indeed, height-for-age deficit is currently considered the most important nutritional problem faced by developing countries.In Brazil, 6 % of children aged less than 5 years suffer from height-for-age deficit,...

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Nutritional programming of disease: unravelling the mechanism

Cited by 184 publications

References 113 publications

Prenatal nicotine exposure enhances the susceptibility to metabolic syndrome in adult offspring rats fed high-fat diet via alteration of HPA axis-associated neuroendocrine metabolic programming

Prenatal nicotine exposure enhances the susceptibility to metabolic syndrome in adult offspring rats fed high-fat diet via alteration of HPA axis-associated neuroendocrine metabolic programming

Serotonin controlling feeding and satiety

A 15-year study on the treatment of undernourished children at a nutrition rehabilitation centre (CREN), Brazil

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