Early weight gain and behavioral responsivity as predictors of dietary obesity in rats

Abstract Background Childhood obesity remains a significant public health problem. To date, most research on the causes and correlates of obesity has focused on a small number of direct predictors of obesity rather than testing complex models that address the multifactorial nature of the origins of obesity in early development. We describe the rationale and methods of iGrow (Infant Growth and Development Study) which will test multiple pathways by which (a) prenatal maternal psychobiological risk predicts infant weight gain over the first 6 months of life, and (b) this early weight gain confers risk for obesity at age 2. Infant hormonal and psychobiological risk are proposed mediators from prenatal risk to early weight gain, though these are moderated by early maternal sensitivity and obesogenic feeding practices. In addition, higher maternal sensitivity and lower obesogenic feeding practices are proposed predictors of adaptive child self-regulation in the second year of life, and all three are proposed to buffer/reduce the association between high early infant weight gain and obesity risk at age 2. Methods iGrow is a prospective, longitudinal community-based study of 300 diverse mothers and infants to be followed across 5 data waves from pregnancy until children are age 2. Key measures include (a) maternal reports of demographics, stress, well-being, feeding practices and child characteristics and health; (b) direct observation of maternal and infant behavior during feeding, play, and distress-eliciting tasks during which infant heart rate is recorded to derive measures of vagal withdrawal; (c) anthropometric measures of mothers and infants; and (d) assays of maternal prenatal blood and infant saliva and urine. A host of demographic and other potential confounds will be considered as potential covariates in structural equation models that include tests of mediation and moderation. Efforts to mitigate the deleterious effects of COVID-19 on study success are detailed. Discussion This study has the potential to inform (1) basic science about early life processes casually related to childhood obesity and (2) development of targeted intervention and prevention approaches that consider mother, infant, and family risks and resources.

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The lambing period of mountain sheep: synthesis, hypotheses, and tests

Canadian Journal of Zoology ◽

10.1139/z82-001 ◽

1982 ◽

Vol 60 (1) ◽

pp. 1-14 ◽

Cited By ~ 62

Author(s):

Fred L. Bunnell

Keyword(s):

Body Weight ◽

Thermal Stress ◽

Weight Gain ◽

Female Body ◽

Extreme Environments ◽

Growth Patterns ◽

Central Tendency ◽

Seasonal Growth ◽

Early Weight Gain ◽

Definition Of

Data on lambing periods from 30 populations of North American mountain sheep are reviewed. Among all populations lambing begins later and duration is shorter at more northern altitudes (p < 0.00006). Correlations are enhanced (p < 0.00003) when latitude is replaced by a phenological index incorporating altitude. Termination of lambing is not correlated with latitude or with phenological index. Two broad patterns are evident. Populations feeding on vegetation of less predictable growth patterns ("desert type") have lengthy lambing seasons; populations feeding on vegetation exhibiting more predictable growth patterns ("alpine type") have shorter lambing seasons, typically two oestrous cycles in length. Definition of "types" by latitude or sheep taxonomy reveals significant differences in lambing periods, but correlations are enhanced when "types" are defined on the basis of habitat.Among taxa, birth weights are correlated with female body weight (rs = 0.87). Birth weights are heavier in extreme environments, seasonal growth patterns are expressed better in the alpine type, and early weight gain is most rapid in the northernmost subspecies. All populations show a strong central tendency with regard to peak lambing (17 May ± 6.8 days). Departures from that tendency respond more to predictability of vegetation than to thermal stress or predation pressure.

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Nucleus accumbens cytoarchitecture predicts weight gain in children

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.2007918117 ◽

2020 ◽

Vol 117 (43) ◽

pp. 26977-26984 ◽

Cited By ~ 1

Author(s):

Kristina M. Rapuano ◽

Jennifer S. Laurent ◽

Donald J. Hagler ◽

Sean N. Hatton ◽

Wesley K. Thompson ◽

...

Keyword(s):

Weight Gain ◽

Nucleus Accumbens ◽

Waist Circumference ◽

Eating Behaviors ◽

Saturated Fat ◽

Brain Regions ◽

Cellular Density ◽

Unhealthy Eating ◽

Early Weight Gain ◽

Prevalence Of Obesity

The prevalence of obesity in children and adolescents worldwide has quadrupled since 1975 and is a key predictor of obesity later in life. Previous work has consistently observed relationships between macroscale measures of reward-related brain regions (e.g., the nucleus accumbens [NAcc]) and unhealthy eating behaviors and outcomes; however, the mechanisms underlying these associations remain unclear. Recent work has highlighted a potential role of neuroinflammation in the NAcc in animal models of diet-induced obesity. Here, we leverage a diffusion MRI technique, restriction spectrum imaging, to probe the microstructure (cellular density) of subcortical brain regions. More specifically, we test the hypothesis that the cell density of reward-related regions is associated with obesity-related metrics and early weight gain. In a large cohort of nine- and ten-year-olds enrolled in the Adolescent Brain Cognitive Development (ABCD) study, we demonstrate that cellular density in the NAcc is related to individual differences in waist circumference at baseline and is predictive of increases in waist circumference after 1 y. These findings suggest a neurobiological mechanism for pediatric obesity consistent with rodent work showing that high saturated fat diets increase gliosis and neuroinflammation in reward-related brain regions, which in turn lead to further unhealthy eating and obesity.

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Psychotropic drug-induced genetic-epigenetic modulation of CRTC1 gene is associated with early weight gain in a prospective study of psychiatric patients

Clinical Epigenetics ◽

10.1186/s13148-019-0792-0 ◽

2019 ◽

Vol 11 (1) ◽

Cited By ~ 1

Author(s):

Aurélie Delacrétaz ◽

Anaïs Glatard ◽

Céline Dubath ◽

Mehdi Gholam-Rezaee ◽

Jose Vicente Sanchez-Mut ◽

...

Keyword(s):

Weight Gain ◽

Side Effects ◽

Prospective Study ◽

Psychotropic Drugs ◽

Energy Homeostasis ◽

Psychiatric Patients ◽

Metabolic Disturbances ◽

Drug Induced ◽

Metabolic Side Effects ◽

Early Weight Gain

Abstract Background Metabolic side effects induced by psychotropic drugs represent a major health issue in psychiatry. CREB-regulated transcription coactivator 1 (CRTC1) gene plays a major role in the regulation of energy homeostasis and epigenetic mechanisms may explain its association with obesity features previously described in psychiatric patients. This prospective study included 78 patients receiving psychotropic drugs that induce metabolic disturbances, with weight and other metabolic parameters monitored regularly. Methylation levels in 76 CRTC1 probes were assessed before and after 1 month of psychotropic treatment in blood samples. Results Significant methylation changes were observed in three CRTC1 CpG sites (i.e., cg07015183, cg12034943, and cg 17006757) in patients with early and important weight gain (i.e., equal or higher than 5% after 1 month; FDR p value = 0.02). Multivariable models showed that methylation decrease in cg12034943 was more important in patients with early weight gain (≥ 5%) than in those who did not gain weight (p = 0.01). Further analyses combining genetic and methylation data showed that cg12034943 was significantly associated with early weight gain in patients carrying the G allele of rs4808844A>G (p = 0.03), a SNP associated with this methylation site (p = 0.03). Conclusions These findings give new insights on psychotropic-induced weight gain and underline the need of future larger prospective epigenetic studies to better understand the complex pathways involved in psychotropic-induced metabolic side effects.

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Diet-induced adipocyte number increase in adult rats: a new model of obesity.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1978.235.3.e279 ◽

1978 ◽

Vol 235 (3) ◽

pp. E279 ◽

Cited By ~ 35

Author(s):

I M Faust ◽

P R Johnson ◽

J S Stern ◽

J Hirsch

Keyword(s):

Adipose Tissue ◽

Weight Gain ◽

Cell Number ◽

Chow Diet ◽

Adipocyte Size ◽

Adult Rats ◽

Tissue Morphology ◽

Number Increase ◽

Dietary Obesity ◽

Morphology Changes

Adult rats of various strains became obese when they were fed a highly palatable diet for several months. Analysis of their adipose tissue morphology revealed increases in both adipocyte size and number in most depots. Reintroduction of an ordinary chow diet to such animals precipitated a period of weight loss during which only mean adipocyte size returned to normal. Adipocyte number remained at the elevated level achieved during the period of weight gain. Thus, transient dietary obesity in rats results in a persistent obesity of a purely hyperplastic, nonhypertrophic form. Furthermore, the persistence of the cell number increase suggests that it is the result of proliferation or differentiation rather than of only an increase in the lipid content of a pool of very small and normally undetected adipocytes. An analysis of adipose tissue morphology changes during the course of diet-induced weight gain suggests that the achievement of some specific mean adipocyte size triggers the events that culminate in adipocyte number increase. What mechanisms may link adipocyte size to the formation of new adipocytes remains unknown.

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