scholarly journals Obesogenic Programming Effects during Lactation: A Narrative Review and Conceptual Model Focusing on Underlying Mechanisms and Promising Future Research Avenues

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 299
Author(s):  
Junilla K. Larsen ◽  
Lars Bode
Keyword(s):  
Human Milk ◽  
High Fat Diet ◽  
Animal Studies ◽  
Maternal Obesity ◽  
Milk Composition ◽  
Future Research ◽  
Weight Outcomes ◽  
Child Eating ◽  
Underlying Mechanisms ◽  
Working Hypotheses

Animal studies have consistently demonstrated that maternal obesity and a high-fat diet during lactation enhances obesity risk in the offspring. However, less is known about these potential obesogenic programming effects in obese humans. We propose three important pathways that may explain obesogenic programming effects of human breastmilk. First, human milk components and hormones may directly affect child eating and satiety characteristics. Second, human milk constituents can affect child microbiota that, in turn, may influence child eating and weight outcomes. Third, human milk composition may affect child eating and weight outcomes through flavor exposure. We reviewed a few very recent findings from well-powered longitudinal or experimental human research with regard to these three pathways. Moreover, we provide a research agenda for future intervention research with the overarching aim to prevent excessive pediatric weight gain during lactation and beyond. The ideas presented in this paper may represent important “black box” constructs that explain obesogenic programming effects during lactation. It should be noted, however, that given the scarcity of studies, findings should be seen as working hypotheses to further test in future research.

scholarly journals Maternal High Fat Diet and in-Utero Metformin Exposure Significantly Impact upon the Fetal Renal Proteome of Male Mice

2019 ◽  
Vol 8 (5) ◽  
pp. 663 ◽  
Author(s):  
Eva Nüsken ◽  
Eva-Maria Turnwald ◽  
Gregor Fink ◽  
Jenny Voggel ◽  
Christopher Yosy ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Maternal Obesity ◽  
Laser Microdissection ◽  
Kidney Tissue ◽  
Standard Diet ◽  
High Fat ◽  
Proteomic Screen ◽  
Eicosanoid Metabolism ◽  
Associated Conditions ◽  
Underlying Mechanisms

There is accumulating evidence for fetal programming of later kidney disease by maternal obesity or associated conditions. We performed a hypothesis-generating study to identify potentially underlying mechanisms. Female mice were randomly split in two groups and fed either a standard diet (SD) or high fat diet (HFD) from weaning until mating and during pregnancy. Half of the dams from both groups were treated with metformin ((M), 380 mg/kg), resulting in four experimental groups (SD, SD-M, HFD, HFD-M). Caesarean section was performed on gestational day 18.5. Fetal kidney tissue was isolated from cryo-slices using laser microdissection methods and a proteomic screen was performed. For single proteins, a fold change ≥1.5 and q-value <0.05 were considered to be statistically significant. Interestingly, HFD versus SD had a larger effect on the proteome of fetal kidneys (56 proteins affected; interaction clusters shown for proteins concerning transcription/translation, mitochondrial processes, eicosanoid metabolism, H2S-synthesis and membrane remodeling) than metformin exposure in either SD (29 proteins affected; clusters shown for proteins involved in transcription/translation) or HFD (6 proteins affected; no cluster). By further analysis, ATP6V1G1, THY1, PRKCA and NDUFB3 were identified as the most promising candidates potentially mediating reprogramming effects of metformin in a maternal high fat diet.

scholarly journals Maternal obesity and the human milk metabolome: associations with infant body composition and postnatal weight gain

2019 ◽  
Vol 110 (1) ◽  
pp. 111-120 ◽  
Author(s):  
Elvira Isganaitis ◽  
Sarah Venditti ◽  
Tucker J Matthews ◽  
Carles Lerin ◽  
Ellen W Demerath ◽  
...  
Keyword(s):  
Body Composition ◽  
Weight Gain ◽  
Childhood Obesity ◽  
Human Milk ◽  
False Discovery Rate ◽  
Maternal Obesity ◽  
Milk Composition ◽  
False Discovery ◽  
Postnatal Weight Gain ◽  
Maternal Bmi

ABSTRACTBackgroundMaternal obesity is a risk factor for childhood obesity; this is a major public health concern given that ∼40% of pregnant women are either overweight or obese. Whether differences in milk composition in lean compared with obese women contribute to childhood obesity is unclear.ObjectivesWe aimed to analyze relationships between maternal obesity and human milk metabolites, infant body composition, and postnatal weight gain.MethodsThis was a prospective study in which mothers intending to breastfeed exclusively, and their newborn infants, were enrolled at delivery (n = 35 mother–infant pairs). We excluded mothers with diabetes, other medical conditions, or pregnancy complications. Participants were grouped by maternal prepregnancy BMI <25 (lean) or ≥25 kg/m2 (overweight/obese). We analyzed infant body composition by dual-energy X-ray absorptiometry and used untargeted liquid chromatography–gas chromatography–mass spectrometry to measure the milk content of 275 metabolites at 1 and 6 mo postpartum.ResultsAt 1 mo postpartum, 10 metabolites differed between overweight/obese and lean groups with nominal P < 0.05, but none was altered with a false discovery rate <0.25. Many differentially abundant metabolites belonged to the same chemical class; e.g., 4/10 metabolites were nucleotide derivatives, and 3/10 were human milk oligosaccharides. Milk adenine correlated positively with both continuously distributed maternal BMI and with infant adiposity and fat accrual. Analysis of milk composition at 6 mo postpartum revealed 20 differentially abundant metabolites (P < 0.05) in overweight/obese compared with lean women, including 6 metabolites with a false discovery rate of <0.25. At both 1 and 6 mo, human milk abundance of 1,5-anhydroglucitol, which has not previously been described in milk, was positively associated with maternal BMI.ConclusionsMaternal obesity is associated with changes in the human milk metabolome. While only a subset of metabolites correlated with both maternal and infant weight, these point to potential milk-dependent mechanisms for mother–child transmission of obesity. This trial was registered at www.clinicaltrials.gov as NCT02535637.

scholarly journals A Mediterranean Meal Plan Modulates Human Milk Composition in Women With Obesity

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 818-818
Author(s):  
Clark Sims ◽  
Audrey , Martinez ◽  
Aline Andres
Keyword(s):  
Human Milk ◽  
Dietary Intervention ◽  
Maternal Obesity ◽  
Post Partum ◽  
Milk Composition ◽  
Healthy Eating Index ◽  
Fat Intake ◽  
Post Intervention ◽  
Meal Plan ◽  
The Impact

Abstract Objectives Human milk (HM) is impacted by both maternal obesity and diet. HM from women with obesity has higher fat, leptin and insulin concentrations. Additionally, maternal dietary fat intake is associated with increased HM fat content. The objective of this study was to determine the impact of a Mediterranean meal plan on the composition of HM from women with obesity. Methods In this pilot study, thirteen women with obesity (body mass index (BMI) ≥ 30 kg/m2) enrolled at five months post-partum and followed a provided Mediterranean meal plan focused on reducing fat intake and increasing unsaturated fat and fiber intake for four weeks. Participants’ diet was assessed using Nutrition Data System for Research. HM was collected at baseline and after the 4-week intervention and the concentrations of metabolites, hormones and cytokines were assayed. Wilcoxon signed-rank tests and analysis of variance were used to assess changes in participant diet and HM composition. Summary statistics are presented as mean ± standard deviation. Results The participants’ Healthy Eating Index Score, a measure of diet quality, significantly improved (38.3 ± 5.13 vs. 78.2 ± 6.75, p &lt; 0.001) and total fat intake was significantly lower (99.6 ± 23.3 g vs. 66.9 ± 12.0 g/day, p &lt; 0.001) after the intervention. Human milk leptin (694 ± 464 pg/ml vs. 437 ± 324 pg/ml, p = 0.007) and tumor necrosis factor α (0.515 ± 0.267 pg/ml vs. 0.310 ± 0.127 pg/ml, p = 0.010) concentrations were lower post intervention, whereas HM macronutrient composition was unchanged. The concentrations of several individual human milk oligosaccharides (HMO) and total HMOs (7720 ± 797 nmol/ml vs. 6986 ± 940 nmol/ml, p = 0.049), as well as HM tyrosine concentration (18.2 ± 6.16 nmol/ml vs. 14.5 ± 4.69 nmol/ml, p = 0.005) were significantly lower post intervention. Conclusions The composition of HM from women with obesity can be modulated by short-term adherence to a Mediterranean meal pattern. These findings merit further studies that use longer interventions and examine the impact of any changes in HM composition on infant growth and development. Modifying HM composition via a dietary intervention may provide a novel strategy to promote child development and health. Funding Sources USDA ARS #6026-51,000-010-05S and #6026-51,000-012-06S, NIH/NIDDK R01DK107516, Arkansas Children's Research Institute/Arkansas Biosciences Institute GR037121.

scholarly journals Maternal adiposity alters the human milk metabolome: associations between nonglucose monosaccharides and infant adiposity

2020 ◽  
Vol 112 (5) ◽  
pp. 1228-1239
Author(s):  
Jessica L Saben ◽  
Clark R Sims ◽  
Brian D Piccolo ◽  
Aline Andres
Keyword(s):  
Human Milk ◽  
Maternal Obesity ◽  
Shikimic Acid ◽  
Milk Composition ◽  
Normal Weight ◽  
Mixed Effect ◽  
Infant Outcomes ◽  
Mixed Effect Models ◽  
Maternal Adiposity ◽  
Linear Mixed Effect Models

ABSTRACT Background Human milk composition is altered by maternal obesity. The association between milk metabolites and infant outcomes has not been thoroughly investigated. Objectives This study aimed to quantify maternal adiposity-related differences in the human milk metabolome and to identify metabolites associated with infant adiposity during the first 6 mo postpartum using untargeted metabolomics. Method Maternal anthropometrics were assessed ≤14 weeks of gestation. Human milk samples were collected at 0.5 mo (n = 159), 2 mo (n = 131), and 6 mo (n = 94) postpartum from normal weight (NW, BMI = 18.5–24.9 kg/m2) and obese (OB, BMI &gt;30 kg/m2) mothers. GC-time-of-flight-MS was used to identify metabolic signatures that discriminate NW and OB women. Partial least squared (PLS)-discriminant analysis, and PLS-regression models were assessed to examine relations between metabolites and maternal BMI and fat mass. Metabolites altered by maternal obesity were used in linear mixed effect models to predict infant adiposity. Results Multivariate modeling identified 23, 17, and 10 metabolites that described maternal adiposity indices at 0.5 mo, 2 mo, and 6 mo postpartum, respectively. Monosaccharides and sugar alcohols were the most representative annotated metabolite classes that were increased in milk from OB women and included: mannose, ribose, lyxose, lyxitol (0.5 mo); mannose, ribitol, glycerol, isothreonic acid, lyxitol (2 mo); lyxitol and isothreonic acid (6 mo). Other discriminant metabolites included: 1-monostearin, xylonolactone, shikimic acid, pseudo uridine, and dodecanol (0.5 mo); N-acetyl-D-hexosamine and fumaric acid (2 mo); uric acid and tyrosine (6 mo). Mannose, lyxitol, and shikimic acid predicted higher infant adiposity over the first 6 mo of life. Conclusions This study reports on 1 of the largest cohorts to date examining the metabolic profiles in human milk comparing NW and OB women. Maternal adiposity was associated with increased amounts of milk nonglucose monosaccharides. Human milk metabolomics may be useful in predicting infant adiposity. These trials were registered at www.clinicaltrials.gov as NCT01131117 and NCT02125149.

060. OVER FEEDING EARLY IN LIFE AND RISK OF OBESITY: INSIGHT FROM THE RODENT

2009 ◽  
Vol 21 (9) ◽  
pp. 15
Author(s):  
M. J. Morris
Keyword(s):  
High Fat Diet ◽  
Animal Studies ◽  
Energy Homeostasis ◽  
Maternal Obesity ◽  
Obesity Risk ◽  
High Fat ◽  
Generational Effects ◽  
Hypothalamic Regulation ◽  
The Impact ◽  
Detrimental Impact

While adult lifestyle factors undoubtedly contribute to the incidence of obesity and its attendant disorders, mounting evidence suggests that programming of obesity may occur following over-nutrition during development. As hypothalamic control of appetite and energy expenditure is set early in life and can be perturbed by certain exposures such as under-nutrition and altered metabolic and hormonal signals, in utero exposure to maternal obesity related changes may contribute to programming of obesity in offspring. Data from animal studies indicate both intrauterine and postnatal environments are critical determinants of the development of pathways regulating energy homeostasis. Experimental evidence in rat studies from our laboratory points to an additive detrimental impact of high fat diet consumption after weaning in animals born of obese mothers. Deleterious effects of high fat diet during pregnancy on metabolic profile, adiposity and cardiac hypertrophy were enhanced by postnatal over consumption. Even modest early postnatal overfeeding induced by litter size reduction leads to increased adiposity. Studies are needed to determine to what extent the effect of maternal and early nutritional changes persist. This presentation summarizes recent evidence of the impact of maternal obesity on subsequent obesity risk, paying particular attention to the hypothalamic regulation of appetite, and markers of metabolic control. There is an urgent need to investigate the mechanisms underlying the trans-generational effects of maternal obesity due to an extraordinary rise in the rates of maternal obesity.

scholarly journals Maternal-infant nutrition and development programming of offspring appetite and obesity

2020 ◽  
Vol 78 (Supplement_2) ◽  
pp. 25-31 ◽  
Author(s):  
Mina Desai ◽  
Michael G Ross
Keyword(s):  
High Fat Diet ◽  
Animal Studies ◽  
Maternal Obesity ◽  
Infant Nutrition ◽  
Public Health Problem ◽  
Underlying Mechanism ◽  
The United States ◽  
High Fat ◽  
Obesity Epidemic ◽  
Increased Risk

Abstract In the United States and Mexico, the obesity epidemic represents a significant public health problem. Although obesity is often attributed to a Western-style, high-fat diet and decreased activity, there is now compelling evidence that this, in part, occurs because of the developmental programming effects resulting from exposure to maternal overnutrition. Human and animal studies demonstrate that maternal obesity and high-fat diet result in an increased risk for childhood and adult obesity. The potential programming effects of obesity have been partly attributed to hyperphagia, which occurs as a result of increased appetite with reduced satiety neuropeptides or neurons. However, depending on maternal nutritional status during the nursing period, the programmed hyperphagia and obesity can be exacerbated or prevented in offspring born to obese mothers. The underlying mechanism of this phenomenon likely involves the plasticity of the appetite regulatory center and thus presents an opportunity to modulate feeding and satiety regulation and break the obesity cycle.

scholarly journals Developmental programming of peripheral diseases in offspring exposed to maternal obesity during pregnancy

2020 ◽  
Vol 319 (5) ◽  
pp. R507-R516 ◽  
Author(s):  
Nirajan Shrestha ◽  
Henry C. Ezechukwu ◽  
Olivia J. Holland ◽  
Deanne H. Hryciw
Keyword(s):  
Animal Studies ◽  
Maternal Obesity ◽  
Disease Risk ◽  
Perinatal Outcomes ◽  
Later Life ◽  
Epidemiological Studies ◽  
Reproductive Age ◽  
Offspring Development ◽  
Adverse Pregnancy ◽  
Underlying Mechanisms

Obesity is an increasing global health epidemic that affects all ages, including women of reproductive age. During pregnancy, maternal obesity is associated with adverse pregnancy outcomes that lead to complications for the mother. In addition, maternal obesity can increase the risk of poor perinatal outcomes for the infant due to altered development. Recent research has investigated the effects of maternal obesity on peripheral organ development and health in later life in offspring. In this review, we have summarized studies that investigated the programming effects of maternal obesity before and during pregnancy on metabolic, cardiovascular, immune, and microbiome perturbations in offspring. Epidemiological studies investigating the effects of maternal obesity on offspring development can be complex due to other copathologies and genetic diversity. Animal studies have provided some insights into the specific mechanisms and pathways involved in programming peripheral disease risk. The effects of maternal obesity during pregnancy on offspring development are often sex specific, with sex-specific changes in placental transport and function suggestive that this organ is likely to play a central role. We believe that this review will assist in facilitating future investigations regarding the underlying mechanisms that link maternal obesity and offspring disease risk in peripheral organs.

Formononetin Ameliorates Cognitive Disorder via PGC-1α Pathway in Neuroinflammation Conditions in High-Fat Diet-Induced Mice

2019 ◽  
Vol 18 (7) ◽  
pp. 566-577 ◽  
Author(s):  
Xinxin Fu ◽  
Tingting Qin ◽  
Jiayu Yu ◽  
Jie Jiao ◽  
Zhanqiang Ma ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
High Fat Diet ◽  
Trifolium Pratense ◽  
Amyloid Β ◽  
Cognitive Disorder ◽  
Mechanism Study ◽  
High Fat ◽  
Neuroprotective Effects ◽  
Underlying Mechanisms

Background: Alzheimer’s disease is one of the most common neurodegenerative diseases in many modern societies. The core pathogenesis of Alzheimer’s disease includes the aggregation of hyperphosphorylated Tau and abnormal Amyloid-β generation. In addition, previous studies have shown that neuroinflammation is one of the pathogenesis of Alzheimer’s disease. Formononetin, an isoflavone compound extracted from Trifolium pratense L., has been found to have various properties including anti-obesity, anti-inflammation, and neuroprotective effects. But there are very few studies on the treatment of Alzheimer’s disease with Formononetin. Objective: The present study focused on the protective activities of Formononetin on a high-fat dietinduced cognitive decline and explored the underlying mechanisms. Methods: Mice were fed with HFD for 10 weeks and intragastric administrated daily with metformin (300 mg/kg) and Formononetin (20 and 40 mg/kg). Results: We found that Formononetin (20, 40 mg/kg) significantly attenuated the learning and memory deficits companied by weight improvement and decreased the levels of blood glucose, total cholesterol and triglyceride in high-fat diet-induced mice. Meanwhile, we observed high-fat diet significantly caused the Tau hyperphosphorylation in the hippocampus of mice, whereas Formononetin reversed this effect. Additionally, Formononetin markedly reduced the levels of inflammation cytokines IL-1β and TNF-α in high-fat diet-induced mice. The mechanism study showed that Formononetin suppressed the pro-inflammatory NF-κB signaling and enhanced the anti-inflammatory Nrf-2/HO-1 signaling, which might be related to the regulation of PGC-1α in the hippocampus of high-fat diet -induced mice. Conclusion: Taken together, our results showed that Formononetin could improve the cognitive function by inhibiting neuroinflammation, which is attributed to the regulation of PGC-1α pathway in HFD-induced mice.

Human milk composition and the effects of pasteurisation on activity of components

2021 ◽  
Author(s):  
Syaza Y. Binte Abu Bakar ◽  
Malinda Salim ◽  
Andrew J. Clulow ◽  
Kevin Nicholas ◽  
Ben J. Boyd
Keyword(s):  
Human Milk ◽  
Milk Composition
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