Subsequent Obesity Research Articles

Hypercorticosteronemia induces hyperphagia and obesity in human growth hormone transgenic rats

Hyperphagia and subsequent obesity are important public health issues due to the associated risks of developing serious diseases. Certain stressors play a major role in the development of hyperphagia. In previous studies, we established a line of human growth hormone transgenic (TG) rats that exhibit hyperphagia and obesity from a young age. We recently demonstrated that voluntary running on a running wheel alleviates hyperphagia in TG rats. Wheel running provides environmental enrichment for rodents and plays a role in relieving stress. These results suggested that stress is the major factor inducing hyperphagia in TG rats. Thus, in the present study, we evaluated activation of the hypothalamus–pituitary–adrenal axis. TG rats showed bilateral enlargement of adrenal glands and hypercorticosteronemia, although their hypothalamic CRH level was comparable to that of wild-type (WT) rats. The ACTH-immunoreactive area was larger and the serum ACTH level in the dark phase was higher in TG rats than in WT rats. Adrenalectomy reduced the food intake of TG rats to a level comparable to that in WT rats, and supplying glucocorticoids recurred hyperphagia in TG rats. These treatments did not affect the food intake of WT rats. Rearing TG rats under group housing prevented hyperphagia and hypercorticosteronemia. These results suggest that glucocorticoids are appetite stimulants, and that TG rats exhibit increased sensitivity to the appetite-stimulating effect of glucocorticoids.

Leptin is a potential biomarker of childhood obesity and an indicator of the effectiveness of weight-loss interventions.

Childhood obesity represents a significant public health concern, imposing a substantial burden on the healthcare system. Furthermore, weight-loss programs often exhibit reduced effectiveness in adults who have a history of childhood obesity. Therefore, early intervention against childhood obesity is imperative. Presently, the primary method for diagnosing childhood obesity relies on body mass index (BMI), yet this approach has inherent limitations. Leptin, a satiety hormone produced by adipocytes, holds promise as a superior tool for predicting both childhood and subsequent adulthood obesity. In this review, we elucidate the tools employed for assessing obesity in children, delve into the biological functions of leptin, and examine the factors governing its expression. Additionally, we discuss maternal and infantile leptin levels as predictors of childhood obesity. By exploring the relationship between leptin levels and weight loss, we present leptin as a potential indicator of the effectiveness of obesity interventions.

Environmental Phenols and Growth in Infancy: The Infant Feeding and Early Development Study.

Higher mean and rapid increases in body mass index (BMI) during infancy are associated with subsequent obesity and may be influenced by exposure to endocrine-disrupting chemicals such as phenols. In a prospective US-based cohort conducted 2010-2014, we investigated associations between environmental phenol exposures and BMI in 199 infants. We measured seven urinary phenols at ages 6-8 and 12 weeks and assessed BMI z-score at up to 12 study visits between birth and 36 weeks. We examined individual and joint associations of averaged early infancy phenols with level of BMI z-score using mean differences (β [95% confidence intervals (CI)]) and with BMI z-score trajectories using relative risk ratios (RR [95% CI]). Benzophenone-3, methyl and propyl paraben, and all phenols jointly were positively associated with higher mean BMI z-score (0.07 [-0.05, 0.18], 0.10 [-0.08, 0.27], 0.08 [-0.09, 0.25], 0.17 [-0.08, 0.43], respectively). Relative to a Stable trajectory, benzophenone-3, 2,4-dichlorophenol, 2,5-dichlorophenol, and all phenols jointly were positively associated with risk of a Rapid Increase trajectory (1.46 [0.89, 2.39], 1.33 [0.88, 2.01], 1.66 [1.03, 2.68], 1.41 [0.71, 2.84], respectively). Early phenol exposure was associated with a higher mean and rapid increase in BMI z-score across infancy, signaling potential long-term cardiometabolic consequences of exposure.

Long-term consumption of rooibos herbal tea affects hypothalamic neurotransmission and social behavior of adult Sprague–Dawley male rats

Abundant in phenolic compounds, “fermented” rooibos herbal tea (FRHT) improves the cognitive performance and exploration of rats, as well as alters the content of monoamines and amino acids in some brain structures. Here, we aim to extend knowledge about the neurochemical and behavioral outcomes of long-term oral FRHT consumption by examining its impact on hypothalamus functions. FRHTs of different leaf-to-water ratios were given to adult male SD rats for 3 months. Their behavior was evaluated in social interaction test. The concentration of hypothalamic monoamines and amino acids was analyzed by HPLC-ECD whereas BDNF/TrkB by Elisa method. It was shown that sustained FRHT consumption did not affect aggression of the rats but was able to increase social deficits, expressed as diminished total time of contact and shorter active social interaction. Upon biochemical investigation, the changes were primarily linked to serotonergic, glutaminergic, and BDNF/TrkB pathway. Decreased 5-HT and TrkB content in the hypothalamus could be linked with social deficits and suggested positive effect on central energy balance, yet the main body mass of animals in the experiment remained unaffected. On the other hand, the reduced hypothalamic serotonin signaling anticipated the influence on hypothalamic–pituitary–adrenal axis and possible diminution of plasma corticosterone level with subsequent behavioral aftermath and lower obesity risk. Our research contributes toward better understanding of the mechanism of action of rooibos tea and its effects within the central nervous system.Graphical abstract

Maternal Prenatal Depressive Symptoms and Fetal Growth During the Critical Rapid Growth Stage

Fetal growth in the critical rapid growth stage (CRGS) before delivery, approximately between 30 to 37 gestational weeks, carries significant implications for subsequent overweight, obesity, and arterial health. Previous evidence has demonstrated the association between maternal depressive symptoms and fetal growth trajectories from early to late pregnancy, but there remains limited understanding of the association of these symptoms with the longitudinal fetal growth change within the CRGS. To investigate the association between maternal depressive symptoms and fetal growth during the CRGS before delivery. This prospective birth cohort study was conducted from January 2018 to December 2020. Volunteer pregnant women were enrolled in their first trimester of prenatal visits. Women with severe disease before pregnancy and multiple births, fetuses with congenital anomalies, and preterm or postterm births were excluded. This multicenter study was based in 13 hospitals covering 81 counties across 12 cities in Sichuan Province, China. Follow-up visits were performed at the second trimester, the third trimester, and 24 hours after delivery. The analysis was conducted from January to May 2023. Maternal depressive symptoms, as a continuous variable, measured by the Edinburgh Postpartum Depression Scale (EPDS) at a median gestational week of 24 (range, 14 to 27) weeks of gestation. A higher score on the EPDS indicates worse depressive symptoms. The main outcomes included ultrasonography-measured biparietal diameter (BPD), femur length (FL), and abdominal circumference (AC), along with calculated estimated fetal weight (EFW). These parameters were evaluated longitudinally at a median gestational week of 30 (range, 28 to 32) and 37 (range, 35 to 39) weeks. Linear mixed models were used to estimate the associations between maternal depressive symptoms and fetal growth parameters. A total of 2676 mother-offspring dyads were included, in which the mean (SD) age of mothers was 28.0 (4.4) years, and 1294 (48.4%) of the offspring were female. The median (IQR) maternal EPDS score was 5.0 (4.0 to 9.0). After adjustment for confounders, a significant correlation was found between a higher score of depressive symptoms in mothers and a slower rate of fetal growth across FL (β = -0.40; 95% CI, -0.58 to -0.22), AC (β = -1.97; 95% CI, -2.90 to -1.03), and EFW (β = -50.11; 95% CI, -68.46 to -31.75). These associations were stronger in female fetuses or those with better family socioeconomic conditions. In this prospective cohort study, maternal depressive symptoms were associated with slower fetal growth rate in the CRGS before delivery. Early screening for depressive disorders in pregnant women appears to be essential for fetal growth and later health.

A newly identified compound activating UCP1 inhibits obesity and its related metabolic disorders.

Promoting thermogenesis in adipose tissue has been a promising strategy against obesity and related metabolic complications. We aimed to identify compounds that promote thermogenesis in adipocytes and to elucidate their functions and roles in metabolism. To identify compounds that directly promote thermogenesis from a structurally diverse set of 4800 compounds, we utilized a cell-based platform for high-throughput screening that induces uncoupling protein 1 (Ucp1) expression in adipocytes. We identified one candidate compound that activates UCP1. Additional characterization of this compound revealed that it induced cellular thermogenesis in adipocytes with negligible cytotoxicity. In a subsequent diet-induced obesity model, mice treated with this compound exhibited a slower rate of weight gain, improved insulin sensitivity, and increased energy expenditure. Mechanistic studies have revealed that this compound increases mitochondrial biogenesis by elevating maximal respiration, which is partly mediated by the protein kinase A (PKA)-p38 mitogen-activated protein kinase (MAPK) signaling pathway. A further comprehensive genetic analysis of adipocytes treated with these compounds identified two novel UCP1-dependent thermogenic genes, potassium voltage-gated channel subfamily C member 2 (Kcnc2) and predicted gene 5627 (Gm5627). The identified compound can serve as a potential therapeutic drug for the treatment of obesity and its related metabolic disorders. Furthermore, our newly clarified thermogenic genes play an important role in UCP1-dependent thermogenesis in adipocytes.

Polygenic Risk Scores and the Risk of Childhood Overweight/Obesity in Association With the Consumption of Sweetened Beverages: A Population-Based Cohort Study.

Background: Sugar-sweetened beverage (SSB) and non-nutritive sweetened beverage (NNSB) consumption is associated with obesity and are targets for population-level dietary interventions. In children (<16 years), we evaluate whether SSB or NNSB consumption is associated with subsequent (2 years later) overweight and/or obesity, and the effect of consumption on subsequent overweight/obesity differs by BMI polygenic risk score (BMI-PRS). Methods: The nationally representative Longitudinal-Study-of-Australian-Children had biennial data collection from birth (n = 5107) until age 14/15 years (n = 3127). At age 11/12 years, a comprehensive biomedical assessment, including PRS assessment, was undertaken (n = 1422). Parent- or self-reported beverage consumption (SSBs: soft drinks, energy drinks, and/or juice; NNSBs: diet drinks) was measured as any/none over previous 24 hours. BMI-PRS was derived using published results (high PRS ≥75th percentile). At ages 4/5-14/15 children were classified as having obesity, overweight/obesity, or not having overweight/obesity using BMI z-score (CDC cut points). Results: SSB consumption had limited association with subsequent overweight/obesity. NNSB consumption was associated with ∼8% more children with subsequent overweight/obesity at most ages. In older children with high BMI-PRS, associations between NNSB consumption and subsequent overweight/obesity strengthened with age [at age 14-15 for high BMI-PRS, difference in proportion with overweight/obesity among NNSB consumers vs. nonconsumers = 0.38 (95% confidence interval: 0.22 to 0.55, p ≤ 0.001)]. There was limited association between SSB consumption and BMI-PRS. Conclusion: NNSB consumption was associated with increased risk of overweight/obesity for children with greater genetic risk at older ages (12-15 years). Focused intervention among children with high genetic risk could target NNSB consumption; however, reverse causality (children with genetic risk and/or high BMI consume more NNSBs) cannot be excluded.

Brain-derived neurotrophic factor knock-out mice develop non-alcoholic steatohepatitis.

While brain-derived neurotrophic factor (BDNF), which is a growth factor associated with cognitive improvement and the alleviation of depression symptoms, is known to regulate food intake and body weight, the role of BDNF in peripheral disease is not fully understood. Here, we show that reduced BDNF expression is associated with weight gain and the chronic liver disease non-alcoholic steatohepatitis (NASH). At 10 months of age, BDNF-heterozygous (BDNF+/- ) mice developed symptoms of NASH: centrilobular/perivenular steatosis, lobular inflammation with infiltration of neutrophils, ballooning hepatocytes, and fibrosis of the liver. Obesity and higher serum levels of glucose and insulin - major pathologic features in human NASH - were dramatic. Dying adipocytes were surrounded by macrophages in visceral fat, suggesting that chronic inflammation occurs in peripheral organs. RNA sequencing (RNA-seq) studies of the liver revealed that the most significantly enriched Gene Ontology term involved fatty acid metabolic processes and the modulation of neutrophil aggregation, pathologies that well characterise NASH. Gene expression analysis by RNA-seq also support the notion that BDNF+/- mice are under oxidative stress, as indicated by alterations in the expression of the cytochrome P450 family and a reduction in glutathione S-transferase p, an antioxidant enzyme. Histopathologic phenotypes of NASH were also observed in a knock-in mouse (BDNF+/pro ), in which the precursor BDNF is inefficiently converted into the mature form of BDNF. Lastly, as BDNF reduction causes overeating and subsequent obesity, a food restriction study was conducted in BDNF+/pro mice. Pair-fed BDNF+/pro mice developed hepatocellular damage and showed infiltration of inflammatory cells, including neutrophils in the liver, despite having body weights and blood parameters that were comparable to those of controls. This is the first report demonstrating that reduced BDNF expression plays a role in the pathogenic mechanism of NASH, which is a hepatic manifestation of metabolic syndrome. © 2023 The Pathological Society of Great Britain and Ireland.

A Longitudinal Investigation of the Buffering Effects of Resilience on Body Mass Index in Trauma-Exposed College Students.

College students are at an increased risk for trauma exposure (TE), as well as weight gain and subsequent obesity. Notably, existing research has demonstrated that TE is associated with subsequent obesity. However, there is a dearth of literature looking at this relationship in college students who are at increased risk. Given this increased risk, there is a need to identify protective factors in the wake of TE that may buffer against the adverse impacts of TE on physical health outcomes. As such, the aim of the present study was to examine the relationship between college onset TE on subsequent BMI, and to examine psychological resilience as a buffer in this relationship. Trauma exposed college students (N= 2,281, Mage=18.5, 61.6% female, 50.3% identifying as racial/ethnic minorities) completed measures of TE, weight, height, and resilience. Individuals completed measures at baseline and at spring follow-up time points each year after. Resilience was assessed using the Connor-Davidson Resilience Scale (CD-RISC), and both new onset TE and BMI were assessed at Y2, Y3, and Y4. There was no significant main effect of new onset TE on BMI, nor an interaction between resilience and new onset TE. There was a main effect of resilience on later BMI, whereby those with higher levels of reported resilience reported higher BMI in subsequent years (Y2: B=.36, p<.05; Y3: B= .37= p<.01). The positive association between resilience and BMI is not consistent with our hypotheses. Findings suggest that resilience does not buffer against physical health outcomes.

Adherence to 24-Hour Movement Guidelines in Relation to the Risk of Overweight and Obesity Among Children and Adolescents

PurposeAdherence to overall 24-hour Movement Guidelines (24HGs) has been associated with childhood obesity in cross-sectional studies. However, few longitudinal studies have examined such associations, especially in China. We aimed to explore prospective associations between adherence to recommendations of 24HGs and risks of developing overweight and obesity among children and adolescents. MethodsWe included participants (aged 6–17 years) without overweight and obesity at enrollment from the China Health and Nutrition Survey in 2004–2011 surveys and followed them till 2015. We assigned one point each to the adherence of guidelines for moderate-to-vigorous physical activity, recreational screen time and sleep, and summed them up to indicate the overall level of adherence to 24HGs (range: 0–3 points). The primary outcome was the first occurrence of overweight or obesity. Multivariable cox proportional hazard models were used to evaluate the corresponding associations. ResultsAmong 1,382 participants (mean age: 10.3 ± 3.2 years; 48.4% girls), a total of 152 (11%) individuals were identified as incident overweight and obesity during an average of 4.7 years of follow-up. Compared with participants nonadherent to any of the guidelines, those adhering to one (hazard ratio [HR] = 0.38, 95% confidence interval [CI]: 0.21–0.71, p < .01), two (HR = 0.49, 95% CI: 0.28–0.88, p = .02), and three (HR = 0.40, 95% CI: 0.17–0.91, p = .03) recommendations had significantly lower risks of developing overweight and obesity. DiscussionChildren and adolescents who met any recommendations of 24HGs had significantly lower risks of developing subsequent overweight and obesity. Setting achievable goals such as adopting at least one recommendation could be considered in future public health recommendations to accelerate progress in childhood obesity prevention.

Dietary Fat Modulation of Gut Microbiota and Impact on Regulatory Pathways Controlling Food Intake.

Obesity is a multifactorial disease that continues to increase in prevalence worldwide. Emerging evidence has shown that the development of obesity may be influenced by taxonomic shifts in gut microbiota in response to the consumption of dietary fats. Further, these alterations in gut microbiota have been shown to promote important changes in satiation signals including gut hormones (leptin, ghrelin, GLP-1, peptide YY and CCK) and orexigenic and anorexigenic neuropeptides (AgRP, NPY, POMC, CART) that influence hyperphagia and therefore obesity. In this review, we highlight mechanisms by which gut microbiota can influence these satiation signals both locally in the gastrointestinal tract and via microbiota-gut-brain communication. Then, we describe the effects of dietary interventions and associated changes in gut microbiota on satiety signals through microbiota-dependent mechanisms. Lastly, we present microbiota optimizing therapies including prebiotics, probiotics, synbiotics and weight loss surgery that can help restore beneficial gut microbiota by enhancing satiety signals to reduce hyperphagia and subsequent obesity. Overall, a better understanding of the mechanisms by which dietary fats induce taxonomical shifts in gut microbiota and their impact on satiation signaling pathways will help develop more targeted therapeutic interventions in delaying the onset of obesity and in furthering its treatment.

Mental Health and Feeding Styles in Parents of Formula-Fed Infants.

Background: Nonresponsive feeding styles can contribute to rapid weight gain in infancy and subsequent obesity in childhood. There is a need to investigate factors such as parental mental health symptoms (stress, depression, and anxiety) that may contribute to nonresponsive feeding styles. The purpose of this study was to investigate the relationship between parental mental health symptoms and feeding styles in parents of healthy, term formula-fed infants during the first year of life. Methods: A cross-sectional, descriptive correlational design was employed using online surveys. We recruited participants through Facebook groups and pediatricians' offices. Instruments included a demographic questionnaire, the Perceived Stress Scale-10, Patient Health Questionnaire-Depression Module-9, 7-item Generalized Anxiety Disorder Assessment, and Infant Feeding Style Questionnaire. Results: Participants were 306 parents of formula-fed infants. Greater depressive symptoms was the strongest predictor of the pressuring style (β = 0.54), while greater symptoms of stress (β = -0.13) and anxiety (β = -0.28) were associated with lower pressuring scores. Greater depressive symptoms was the strongest predictor of the laissez-faire style (β = 0.48), while greater symptoms of stress (β = -0.17) and anxiety (β = -0.23) were associated with lower laissez-faire scores. Engaging in ≤50% of the infant's feeds was the strongest control variable predictor for the pressuring and laissez-faire styles. None of the mental health variables were significantly related to the restrictive style. Conclusions: We recommend increased screening for depressive symptoms in parents of infants and responsive feeding support, especially for those experiencing depressive symptoms.

High density lipoprotein-associated proteins in non-obese women with and without polycystic ovary syndrome.

Dyslipidemia frequently occurs in women with polycystic ovary syndrome (PCOS), but it is unclear whether dyslipidemia is due to obesity and insulin resistance (IR) or is inherent to PCOS. To address this, proteomic analysis of proteins important in lipid metabolism, particularly for high-density lipoprotein cholesterol (HDL-C), was performed in non-obese, non-insulin resistant PCOS women compared to matched controls. Weight and aged-matched non-obese subjects with PCOS (n=24) and without IR were compared with control women (n=24). 19 proteins were measured by Somalogic proteomic analysis: alpha-1-antichymotrypsin, alpha-1-antitrypsin, apolipoproteins A-1, B, D, E, E2, E3, E4, L1, M, clusterin, complement C3, hemopexin, heparin cofactor-II (HCFII), kininogen-1, serum amyloid A-1, amyloid beta A-4 and paraoxonase-1. Women with PCOS had a higher free androgen index (FAI) (p<0.001) and anti-Mullerian hormone (AMH) (p<0.001), but IR and C-reactive protein (CRP), a marker of inflammation, did not differ from controls (p>0.05). The triglyceride:HDL-cholesterol ratio was elevated (p=0.03) in PCOS. Alpha-1-antitrypsin levels were lower (p<0.05) and complement C3 levels were higher (p=0.001) in PCOS. C3 correlated with body mass index (BMI) (r=0.59, p=0.001), IR (r=0.63, p=0.0005) and CRP (r=0.42, p=0.04) in women with PCOS, though no correlations of these parameters with alpha-1-antitrypsin were found. Total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol and levels of the other 17 lipoprotein metabolism-associated proteins did not differ between the two groups (p>0.05). However, in PCOS, alpha-1-antichymotrypsin correlated negatively with BMI (r=-0.40, p<0.04) and HOMA-IR (r=-0.42, p<0.03), apoM correlated positively with CRP (r=0.36, p<0.04) and HCFII correlated negatively with BMI (r=-0.34, p<0.04). In PCOS subjects, when obesity, IR and inflammation confounders were absent, alpha-1-antitrypsin was lower and complement C3 was higher than in non-PCOS women, suggesting increased cardiovascular risk; however, subsequent obesity related IR/inflammation likely stimulates other HDL-associated protein abnormalities, thus increasing cardiovascular risk further.

A Single Bout of Remote Ischemic Preconditioning Suppresses Ischemia-Reperfusion Injury in Asian Obese Young Men.

Remote ischemic preconditioning (RIPC) has been shown to minimize subsequent ischemia-reperfusion injury (IRI), whereas obesity has been suggested to attenuate the efficacy of RIPC in animal models. The primary objective of this study was to investigate the effect of a single bout of RIPC on the vascular and autonomic response after IRI in young obese men. A total of 16 healthy young men (8 obese and 8 normal weight) underwent two experimental trials: RIPC (three cycles of 5 min ischemia at 180 mmHg + 5 min reperfusion on the left thigh) and SHAM (the same RIPC cycles at resting diastolic pressure) following IRI (20 min ischemia at 180 mmHg + 20 min reperfusion on the right thigh). Heart rate variability (HRV), blood pressure (SBP/DBP), and cutaneous blood flow (CBF) were measured between baseline, post-RIPC/SHAM, and post-IRI. The results showed that RIPC significantly improved the LF/HF ratio (p = 0.027), SBP (p = 0.047), MAP (p = 0.049), CBF (p = 0.001), cutaneous vascular conductance (p = 0.003), vascular resistance (p = 0.001), and sympathetic reactivity (SBP: p = 0.039; MAP: p = 0.084) after IRI. However, obesity neither exaggerated the degree of IRI nor attenuated the conditioning effects on the measured outcomes. In conclusion, a single bout of RIPC is an effective means of suppressing subsequent IRI and obesity, at least in Asian young adult men, does not significantly attenuate the efficacy of RIPC.

Weight-for-age z-scores of Japanese children using the World Health Organization Child Growth Standards.

Weight-for-age z-scores of Japanese children using the World Health Organization Child Growth Standards.

Unique cardiac remodeling in young adults born Small for Gestational Age with subsequent central obesity

Abstract Background Being born small-for-gestational age (SGA, 10 percent of all births) is associated with increased risk of cardiovascular mortality (1,2) in adulthood together with lower exercise tolerance (3), but mechanistic pathways are unclear. Central obesity is known to worsen cardiovascular outcomes, but it is uncertain how it affects the heart in adults born SGA. Purpose We aimed to assess whether central obesity makes young adults born SGA more susceptible to cardiac remodelling and dysfunction. Methods A perinatal cohort study including 80 young adults born SGA (birth weight below 10th centile) and 75 adults with normal birth weight (controls). Current waist-to-hip ratio was used as a surrogate of central obesity. Cardiac structure and function were assessed by cardiac magnetic resonance. Statistical shape analysis was used to study the regional geometric variability of the biventricular surfaces produced by central obesity and SGA, and synthetic surfaces representative of obese and non obese were generated for both SGA and controls. Results Figure 1 shows the superimposed representative surfaces of obese and non-obese according to our model, for controls (right column) and SGA (left column). Both SGA and waist-to-hip were highly associated to cardiac shape (F=3.94 p&amp;lt;0.001; F=5.18 p&amp;lt;0.001 respectively) with a statistically significant interaction (F=2.29, p=0.02), indicating a different cardiac remodelling due to obesity in SGA. While controls tend to increase left ventricular end-diastolic volumes, mass and stroke volume with increasing waist-to-hip ratio, young adults born SGA showed unique response with inability to increase cardiac dimensions or mass resulting in reduced stroke volume (both in absolute values and indexed by body surface area) and increased heart rate. Conclusions SGA young adults show unique cardiac adaptation to central obesity, which is associated with a decrease in stroke volume. Preventive strategies aiming to reduce cardiometabolic risk in SGA population may be warranted. Funding Acknowledgement Type of funding sources: Public grant(s) – EU funding. Main funding source(s): European Union Horizon 2020 Programme

Duodenojejunal Omega Switch Surgery Reduces Oxidative Stress Induced by Cafeteria Diet in Sprague-Dawley Rats.

Over-nutrition with cafeteria diet leads to glycemic control failure and subsequent obesity. Bariatric surgery remains the ultimate treatment option, and when complemented with specific dietary protocol, it may mitigate the effects of oxidative stress induced by a cafeteria diet. The study measured antioxidant marker activity: superoxidase dismutase (SOD) and ceruloplasmin (CER), total antioxidant capacity (TAC), and lipid peroxidation marker concentrations: lipofuscin (LS) and malondialdehyde (MDA), in the plasma of 56 Sprague-Dawley rats fed with a cafeteria (HFS) or a control (CD) diet and subjected to duodenojejunal omega switch (DJOS) or control (SHAM) surgery. The diet change after the surgery (CD/HFS or HFS/CD) strongly influenced SOD activity in DJOS- and SHAM-operated rats, but SOD activity was always higher in SHAM-operated rats. Every dietary protocol used in the study increased CER activity, except for the CD/CD combination. Cafeteria diet consumed before or after either of surgeries led to decrease in TAC levels. DJOS and no change in diet reduced MDA levels. DJOS reduced LS levels, but its beneficial effect was deteriorated by selected dietary protocols. The cafeteria diet negatively affected the positive impact of DJOS surgery, but SOD, CER, MDA, and LS were significantly lower in rats that underwent DJOS, suggesting that eight weeks of dietary treatment before and after the surgery did not totally dilapidate the effects of the bariatric treatment.

Optimising weight gain in pregnancy: key challenges and solutions for maternal obesity prevention.

Pregnancy is a high-risk period for excess gestational weight gain and subsequent obesity development. Antenatal lifestyle interventions are prioritised to optimise weight, with current evidence demonstrating efficacy and associated reduction in risk of adverse maternal and neonatal outcomes. Yet, evidence to guide the field from efficacy-based to implementation research within real-world settings is lacking, and several key challenges remain. Here, we discuss key considerations to support the implementation of accessible, relevant, effective, and low-cost lifestyle interventions in routine pregnancy care. This includes identifying what components of lifestyle interventions are most effective, with pragmatic guidance on how to conduct implementation research, improving rigour in reporting to ensure learnings from implementation are captured, and recognising and addressing the socioecological aspects of obesity prevention, including supporting women living with socioeconomic disadvantage and reducing weight stigma.

Longitudinal exposure to neighborhood poverty and obesity risk in emerging adulthood

This study uses data from the longitudinal Panel Study of Income Dynamics data and its Transition to Adulthood (TA) Study (2005–2017), in conjunction with decades of neighborhood-level data from the U.S. decennial census and American Community Survey, to examine the relationship between individuals’ neighborhood poverty exposure trajectories in childhood and the likelihood of obesity in emerging adulthood. Latent growth mixture models reveal that exposure to neighborhood poverty differs considerably for white and nonwhite individuals over their childhood life course. Durable exposure to neighborhood poverty confers greater subsequent obesity risks in emerging adulthood than transitory experiences of neighborhood poverty. Racial differences in the changing and persistent trajectories of neighborhood poverty help explain part of the racial differences in obesity risks. Among nonwhites, and compared to consistent nonpoor neighborhood conditions, both durable and transitory neighborhood poverty exposures are significantly associated with higher obesity risks. This study suggests that a theoretical framework that integrates key elements of the life-course perspective is helpful to uncover the individual and structural pathways through which neighborhood histories in poverty shape population health in general.

Association of infant diet with subsequent obesity at 2-5 years among children exposed to gestational diabetes: the SWIFT study

Association of infant diet with subsequent obesity at 2-5 years among children exposed to gestational diabetes: the SWIFT study