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Fetal Programming of Food Preferences and Feeding Behavior

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Diet, Nutrition, and Fetal Programming

Abstract

Children that do not reach their full growth potential in utero have an increased risk for developing glucose intolerance, increased adiposity and metabolic syndrome features as adults. As food intake and feeding behavior, along with energy expenditure, are major determinants in the development of such features, it is expected that these individuals will show altered feeding patterns over the life course. However, aside from increased appetite, only recently research has been dedicated to explore the effects that poor fetal growth can have on food preferences. Despite being a new focus of investigation, there is compelling evidence, both clinical and experimental, that exposure to fetal paucity of nutrients may have programming effects on feeding preferences and behaviors that can contribute to the development of diseases. Individuals born small for gestational age (SGA) have preferences towards highly caloric and palatable foods such as carbohydrates and fats, and eventually will display altered eating behaviors as well. These behaviors lead to small but persistent nutrient imbalances across the lifespan, increasing the risk of chronic, non-transmittable diseases in adult life in these individuals. Different animal models of poor fetal growth were developed, allowing a deeper understanding of the mechanisms potentially involved in these findings. Alterations in brain pathways, involved in the search and reward sensations associated with the intake of high palatable foods, such as the mesocorticolimbic dopamine and opioids pathways, as well as their modulators, seem to be involved. We review this evidence, discuss the mechanisms and propose points for future research and possible development of interventions to prevent these altered behaviors in this vulnerable population.

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Abbreviations

AGA:

Adequate for gestational age

AgRP:

Agouti-related peptide

ARC:

Arcuate nucleus

ASST:

Attentional Set-Shifting Task

BMI:

Body mass index

BWR:

Birth weight ratio (birth weight/mean populational birth weight, sex and gestational age specific)

D2:

Dopamine type 2 receptor

DA:

Dopamine

DAT:

Dopamine reuptake transporter

DHA:

Docosahexaenoic acid

fMRI:

Functional magnetic resonance imaging

HOMA-IR:

Homeostatic model assessment for insulin resistance

HPA:

Hypothalamus – pituitary – adrenal

IUGR:

Intrauterine growth restriction

LMPT:

Late and moderately preterm children

LPEarly, LPMid, LPLate:

Low-protein diet in different gestational periods: day 0–7 (LPEarly), day 8–14 (LPMid) or day 15–22 (LPLate)

MOR:

Mu-opioid receptor

n-3 PUFAs:

n-3 polyunsaturated fatty acids

NAcc:

Nucleus accumbens

NPY:

Neuropeptide Y

ObRb:

Leptin receptor

OFC:

Orbitofrontal cortex

PENK:

Preproenkephalin

PFC:

Prefrontal cortex

PI3K:

Phosphoinositide 3-kinase

POMC:

Pro-opiomelanocortin

pTH:

Phospho-tyrosine hydroxylase

SGA:

Small for gestational age

TH:

Tyrosine-hydroxylase

VLBW:

Very low birth weight

VTA:

Ventral tegmental area

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Correspondence to Adrianne Rahde Bischoff MD .

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Bischoff, A.R., DalleMolle, R., Silveira, P.P. (2017). Fetal Programming of Food Preferences and Feeding Behavior. In: Rajendram, R., Preedy, V., Patel, V. (eds) Diet, Nutrition, and Fetal Programming. Nutrition and Health. Humana Press, Cham. https://doi.org/10.1007/978-3-319-60289-9_33

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