Comparison of the Effect of Direct Breastfeeding, Expressed Human Milk, and Infant Formula Feeding on Infant Weight Trajectories: A Systematic Review.

Background: Formula and breastfeeding are known factors associated with infant weight trajectories. Evidence exploring the effect of expressed human milk feeding on infant weight in the community setting has not been well synthesized. Objectives: This systematic review examined (1) weight changes among infants fed expressed human milk and (2) differences in weight change between infants fed expressed human milk and infants fed at the breast or infant formula via bottle. Methods: A comprehensive search of the literature was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The quality of each study was appraised using the Joanna Briggs Critical Appraisal Tools. Results: A total of six studies met the eligibility criteria and included a total of 5,152 infants. The within-subject analysis identified only 31 infants strictly or predominantly fed expressed human milk. The between-subject analysis comparing expressed human milk feeding to the available comparison groups (formula-fed or direct at the breastfed) revealed that higher weight gains were observed in the weight trajectories among infants in the bottle or formula-fed conditions in four of the six included studies. Conclusions: Findings from the few studies included in this review found a difference in the infant weight gain patterns among expressed human milk-fed infants when compared with their respective feeding groups (directly breastfed or formula-fed). Further research is needed to corroborate these findings and elucidate the clinical significance of the differences in weight gain patterns observed across infant feeding groups.

Gestational Weight Gain: Is the Role of Genetic Variants a Determinant? A Review.

Excessive or insufficient gestational weight gain (GWG) leads to diverse adverse maternal and neonatal outcomes. There is evidence that pregestational body mass index (pBMI) plays a role in GWG, but no genetic cause has been identified. In this review, we aim to analyze genotype variants associated with GWG. Results: We identified seven genotype variants that may be involved in GWG regulation that were analyzed in studies carried out in Brazil, Romania, the USA, Turkey, Ukraine, and Canada. Some genetic variants were only associated with GWG in certain races or depending on the pBMI. In women who were obese or overweight before gestation, some genetic variants were associated with GWG. Environmental and genetic factors together showed a greater association with GWG than genetic factors alone; for example, type of diet was observed to have a significant influence. Conclusions: We found little scientific evidence of an association between genotype variants in countries with a high prevalence of women of reproductive age who are overweight and obese, such as in Latin America. GWG may be more dependent on environmental factors than genetic variants. We suggest a deeper study of genetic variants, cytokines, and their possible association with GWG, always with the respective control of potential cofounding factors, such as pBMI, diet, and race.

A macrophage-collagen fragment axis mediates subcutaneous adipose tissue remodeling in mice.

Efficient removal of fibrillar collagen is essential for adaptive subcutaneous adipose tissue (SAT) expansion that protects against ectopic lipid deposition during weight gain. Here, we used mice to further define the mechanism for this collagenolytic process. We show that loss of collagen type-1 (CT1) and increased CT1-fragment levels in expanding SAT are associated with proliferation of resident M2-like macrophages that display increased CD206-mediated engagement in collagen endocytosis compared to chow-fed controls. Blockage of CD206 during acute high-fat diet-induced weight gain leads to SAT CT1-fragment accumulation associated with elevated inflammation and fibrosis markers. Moreover, these SAT macrophages' engagement in collagen endocytosis is diminished in obesity associated with elevated levels collagen fragments that are too short to assemble into triple helices. We show that such short fragments provoke M2-macrophage proliferation and fibroinflammatory changes in fibroblasts. In conclusion, our data delineate the importance of a macrophage-collagen fragment axis in physiological SAT expansion. Therapeutic targeting of this process may be a means to prevent pathological adipose tissue remodeling, which in turn may reduce the risk for obesity-related metabolic disorders.

Association of maternal body mass index change with risk of large for gestational age among pregnant women with and without gestational diabetes mellitus: a retrospective cohort study.

OBJECTIVE: To investigate the associations of body mass index (BMI) change and large for gestational age (LGA) among prepregnancy normal-weight women with and without gestational diabetes mellitus (GDM). METHODS: The retrospective study including 9515 normal-weight pregnant women (1331 women with GDM and 8184 without GDM) was conducted in Fujian Maternity and Child Health Hospital in 2020. The BMI change was calculated as gestational weight gain in kilograms by maternal height in meters. The binary logistic regression, stratified analyses, restricted cubic spline models and additive interaction analysis were adopted to reveal the relationship between BMI change and LGA. RESULTS: Pregnant women with GDM had a lower level of BMI change but a higher incidence of LGA compared with those without GDM. After adjustment for covariates variables, we found that the risk of LGA was associated with the highest quartile of BMI change (OR = 1.89, 95%CI:1.27-2.8 for GDM and OR = 1.48,95%CI:1.27-1.75 for non-GDM). There were significant linear relationships of BMI change and LGA with the inflection point of 5.096 and 5.401 kg/m2 in GDM and non-GDM groups. Significant additive interaction was observed between parity and BMI change level concerning LGA. A significant difference in BMI change and gestational weight gain (GWG) for LGA prediction was detected. CONCLUSION: Higher BMI changes were significantly associated with a higher risk of LGA in pregnant women with or without GDM in a linear dose-response relationship, with the threshold around 5.096 and 5.401 kg/m2, respectively. These suggested that BMI changes may be a useful predictor for the incidence of LGA in singleton pregnant women.

A significant increase in anthropometric indices during long-term follow-up of pediatric patients with celiac disease, with no endocrine disorders.

Celiac disease (CeD) is likely to be associated with growth impairment and poor weight gain. However, long-term growth patterns following diagnosis are poorly characterized. We evaluated long-term anthropometric changes in a large cohort of pediatric patients with CeD. A retrospective chart review of patients diagnosed with CeD between 1999 and 2018 was conducted. Demographic and clinical data were collected, and anthropometrics were analyzed from diagnosis and throughout follow-up. The study included 500 patients (59.8% females, median (IQR) age at diagnosis 5.7 (3.7-8.9) years), with a mean follow-up of 5.5 (range 1.5-16.2) years. Weight, height, and BMI Z-score-for-age (WAZ, HAZ, and BMIZ) increased significantly from a mean (± SD) of - 0.82 (± 1.21), - 0.73 (± 1.16), and - 0.32 (± 1.11) at diagnosis to - 0.41 (± 1.23), - 0.45(± 1.16), and - 0.17 (± 1.14) at last follow-up, respectively (p < 0.001 for WAZ and HAZ and p = 0.002 for BMIZ). The largest improvements were observed in patients diagnosed before 3 years of age (p < 0.01). Patients for whom the final adult height was available (n = 86) improved from HAZ mean (± SD) - 0.89 ± 1.37 at diagnosis to - 0.51 ± 1.28 at adulthood measurement, p < 0.05. Wasting was present in 19.7% and stunting in 16.4% of the cohort at diagnosis and normalized in 77.3% and 64.8%, respectively, within a median (IQR) time of 0.79 (0.42-4.24) and 2.3 (0.72-6.02) years, respectively. Gluten-free diet adherence and frequency of visits were not associated with normalization of wasting or stunting in all age groups.  Conclusion: Over a long-term follow-up, pediatric patients with CeD demonstrate significant increases in weight, height, and BMI-for-age. Younger age at diagnosis is associated with greater improvement in weight and linear growth, emphasizing the importance of early diagnosis of CeD. What is Known: • Celiac disease (СeD) is likely to be associated with growth impairment and poor weight gain. • Long-term changes in anthropometric indices after diagnosis of CeD are not well characterized. What is New: • Over a long-term follow-up, pediatric patients with CeD demonstrate significant increases in weight, height, and BMI-for-age. • Young age at diagnosis is associated with larger improvement in weight and linear growth.

Association of glucose metabolism and insulin resistance with feed efficiency and production traits of finishing beef steers.

Increasing nutrient utilization efficiency is an important component of enhancing the sustainability of beef cattle production. The objective of this experiment was to determine the association of glucose metabolism and insulin resistance with dry matter intake (DMI), average daily gain (ADG), gain:feed ratio (G:F), and residual feed intake (RFI). Steers (n = 54; initial body weight = 518 ±â€…27.0 kg) were subjected to an intravenous glucose tolerance test (IVGTT) where glucose was dosed through a jugular catheter and serial blood samples were collected. Three days after the last group's IVGTT, steers began a 63-d DMI and ADG test. Body weight was measured on days 0, 1, 21, 42, 62, and 63, and DMI was measured using an Insentec Roughage Intake Control system (Hokofarm Group, Emmeloord, the Netherlands). To examine relationships between DMI, ADG, G:F, and RFI with IVGTT measurements, Pearson correlations were calculated using Proc Corr of SAS 9.4 (SAS Inst. Inc., Cary, NC). Additionally, cattle were classified based on DMI, ADG, RFI, and G:F, where the medium classification was set as mean ±â€…0.5 SD, the low classification was < 0.5 SD from the mean, and the high classification was > 0.5 SD from the mean. No associations between DMI and IVGTT parameters were observed, and no differences were detected when classifying cattle as having low, medium, or high DMI. Peak insulin concentration in response to the IVGTT tended to be correlated with ADG (r = 0.28; P = 0.07), indicating cattle with greater ADG tend to have a greater insulin release in response to glucose. Glucose nadir concentrations tended to be positively correlated with ADG (r = 0.26; P = 0.10). Additionally, the glucose nadir was greater in high-ADG steers (P = 0.003). The association of greater glucose nadir with high-ADG could indicate that high-ADG steers do not clear glucose as efficiently as low-ADG steers, potentially indicating increased insulin resistance. Further, RFI was not correlated with IVGTT measurements, but low RFI steers had a greater peak glucose concentration (P = 0.040) and tended to have a greater glucose area under the curve (P = 0.09). G:F was correlated with glucose area under the curve (r = 0.33; P = 0.050), glucose nadir (r = 0.35; P = 0.011), and insulin time to peak (r = 0.39; P = 0.010). These results indicate that glucose metabolism and insulin signaling are associated with growth and efficiency, but the molecular mechanisms that drive these effects need to be elucidated.

Feed efficiency is an important component of improving the sustainability of beef production. There is a need to understand how metabolism influences feed efficiency. This experiment aimed to explore the association of glucose metabolism and insulin resistance with feed intake, growth, and efficiency of finishing beef cattle. The results indicate that there is a relationship between insulin resistance and improved efficiency measured as the ratio of growth to feed intake. The findings of this experiment are novel as they show a relationship between insulin resistance and feed efficiency and indicate further research is needed to determine the mechanisms of insulin resistance in ruminants that contribute to improved feed efficiency.

Weight Gain from Birth to Adolescence and TyG Index at Age 18 Years: A Cohort Study in Northeast Brazil.

BACKGROUND: Developmental models suggest that the phenotypes may arise from an immediate or mediated adaptive metabolic response of the perinatal growth. Evidence on the cumulative effects of growth and factors associated with risk of insulin resistance in adolescents is lacking. OBJECTIVE: To investigate the association between birthweight, weight gain during infancy, childhood and adolescence and the triglyceride-glucose index in adolescents. METHODS: This is a cohort of 217 children born at term, followed for the first six months, and reassessed at 8 and 18 years of age. The variables of interest were birthweight, postnatal growth defined as rapid postnatal growth when the weight gain from birth to six months of age was greater than 0.67 z-score, and the same criterion was used for high BMI gain from ages 6 months to 8 years, and from 8 to 18 years. Socioeconomic condition, nutritional status, practice of physical exercises and consumption of ultra-processed foods were verified. Multivariate linear regression analysis was used to verify the effect of the variables on the triglyceride-glucose index. RESULTS: Birthweight was not associated with triglyceride-glucose index in adolescence. Rapid postnatal growth during the first 6 months, higher BMI gain from 8 to 18 years and higher waist circumference contributed significantly to explain higher triglyceride-glucose index. CONCLUSION FOR PRACTICE: Our findings suggest that rapid postnatal growth may be one of the first signs of a higher triglyceride-glucose index in adolescence and that attention should be paid to the greater gain in body mass between childhood and adolescence for the risk of a higher triglyceride-glucose index.

Comparison of intermittent fasting and voluntary wheel running on physical and cognitive abilities in high-fat diet-induced obese rats.

Regular physical activity is a proven routine for weight management in addressing obesity. Another method that has gained attention for its health benefits is intermittent fasting (IF). Physical and cognitive abilities while on these routines are poorly understood in the obese population. Sixty-five male Sprague Dawley rats at 7 weeks of age were subjected to diet-induced obesity by feeding a high-fat diet (HFD) or a standard diet (SD) for 8 weeks, after which behavioral testing was performed to detect any changes in physical and cognitive abilities. Rats from the HFD-fed (now considered obese) and SD-fed groups were then subjected to IF (18-hour fast and 6-hour feeding daily), voluntary wheel running (VWR), or control conditions for 3 weeks before repeating the same behavioral testing protocol. IF resulted in less weight gain (p<0.05) and elevated ketone levels (p<0.05) in both SD and HFD-fed groups. IF improved physical activity when compared to VWR and control animals in both SD and HFD-fed groups (p<0.05) while the VWR group in the SD-fed rats exhibited less physical fatigue compared to IF and controls (p<0.05). Additionally, elevated ketone levels were weakly correlated with decreased physical (p<0.0001) and exploratory behavior (p<0.01). These results suggest that IF is more effective than VWR in HFD and SD-fed rats in minimizing weight gain and retaining physical activity, and ketones may play a part in establishing the reported physical benefits. Exploration of physiological mechanisms between ketones, diet, and exercise will help fight obesity and many associated diseases.

Behavioral, psychological, and environmental predictors of weight regain in a group of successful weight losers in a widely available weight-management program.

OBJECTIVE: The aim of this study was to identify predictors of weight regain and continued weight maintenance among individuals already successful at long-term weight loss in a widely available weight-management program. METHODS: Participants were 2843 weight-loss maintainers in WeightWatchers who had maintained weight loss ≥9.1 kg for ≥1 year (average 25.5 kg for 3.5 years; BMI = 26.7 kg/m2 ). Validated behavioral, psychosocial, and home environmental questionnaires were administered at study entry and 1 year later. Discriminant analysis identified variables that discriminated gainers (≥2.3-kg gain) from maintainers (±2.3-kg change). RESULTS: Over the 1 year of follow-up, 43% were gainers (mean [SD], 7.2 [5.4] kg), and 57% were maintainers (0.4 [1.2] kg). Compared with maintainers, gainers were younger and had higher initial weight, more recent weight losses, and larger initial weight losses. Standardized canonical coefficients indicated that the 1-year changes that most discriminated gainers from maintainers were greater decreases in the ability to accept uncomfortable food cravings, urges, and desires to overeat (0.232); self-monitoring (0.166); body image (0.363); and body satisfaction (0.194) and greater increases in disinhibition (0.309) and bodily pain (0.147). The canonical correlation was 0.505 (p < 0.001). CONCLUSIONS: Future interventions to prevent regain should consider targeting overeating in response to internal and external food cues and declines in self-monitoring and body image.

[Prevention and management of postinterventional weight regain]. / Prävention und Management von postinterventioneller Gewichtszunahme.

Decreasing levels of patient motivation or compliance are far from being the only causes of postinterventional weight regain after lifestyle, psychological, pharmacological and surgical interventions. Weight regain originates from a complex and individually varying set of central and peripheral mechanisms, with the overall purpose of increasing food intake by both stimulating hunger and reducing satiety (mediated by gastrointestinal hormones) and decreasing the body's energy demands (via metabolic adaption). These mechanisms counteract any attempts to reduce or maintain body weight in today's increasingly prevalent adipogenic environments. The knowledge about the biological mechanisms of body weight regulation should be taken into consideration when planning treatment programs for long-term weight reduction, including follow-up treatment for the prevention and individualized treatment of postinterventional weight regain. Therapeutic measures as well as the frequency of medical follow-ups should be based on the extent of weight regain.

Bone marrow immune cells respond to fluctuating nutritional stress to constrain weight regain.

Weight regain after weight loss is a major challenge in the treatment of obesity. Immune cells adapt to fluctuating nutritional stress, but their roles in regulating weight regain remain unclear. Here, we identify a stem cell-like CD7+ monocyte subpopulation accumulating in the bone marrow (BM) of mice and humans that experienced dieting-induced weight loss. Adoptive transfer of CD7+ monocytes suppresses weight regain, whereas inducible depletion of CD7+ monocytes accelerates it. These cells, accumulating metabolic memories via epigenetic adaptations, preferentially migrate to the subcutaneous white adipose tissue (WAT), where they secrete fibrinogen-like protein 2 (FGL2) to activate the protein kinase A (PKA) signaling pathway and facilitate beige fat thermogenesis. Nevertheless, CD7+ monocytes gradually enter a quiescent state after weight loss, accompanied by increased susceptibility to weight regain. Notably, administration of FMS-like tyrosine kinase 3 ligand (FLT3L) remarkably rejuvenates CD7+ monocytes, thus ameliorating rapid weight regain. Together, our findings identify a unique bone marrow-derived metabolic-memory immune cell population that could be targeted to combat obesity.

Quantitative and molecular aspects of water intake in meat-type chickens.

Even though water is the most essential nutrient for poultry production, adequate data on individual water intake in broiler chickens and its relationship with other traits of economic importance is scant. Water is provided to chickens in an unrestricted manner in spite of being a finite resource. Climate change continues to affect water sources and efficient bird use of water is long overdue. Understanding the biological basis of water intake is essential for sustainability of the poultry industry. Individual water and feed intake, and growth data was collected on 520 commercial broilers aged 14 to 42 days. We introduced the concepts of water conversion ratio (WCR) and residual water intake (RWI) as parameters that can be used to assess water intake efficiency. Water conversion ratio was defined as the amount of water consumed per unit of body weight gain, and RWI was defined as the difference between the actual water intake (WI) of a given bird and the expected WI by an average bird from the population with the same metabolic body weight, feed intake (FI) and body weight gain (BWG). The correlation between WI and FI was positive (r=0.77; P<0.0001), and the correlation between WI and BWG was positive (r=0.80; P<0.0001). Based on the distribution of RWI, the bottom 5 birds (LRWI) and the top 5 birds (HRWI) for RWI were selected for mRNA expression differences. The average broiler consumed about 7.8 L (± 1L) of water from 14 to 42 days of age. The mRNA expression of arginine vasopressin (AVP) antidiuretic hormone, calcium sensing receptor (CasR), sodium channel epithelial 1 subunit alpha (SCNN1A) and SCNN1D in the hypothalamus was upregulated in the LRWI group compared to the HRWI group. Similarly, kidney aquaporins (AQP) 2, 3, and 4 were upregulated in the LRWI group compared with the HRWI group. Given that water was provided ad libitum, the up-regulation of AVP and AQP gene mRNA expressions seem to indicate that the LRWI birds were more efficient in water reabsorption in the kidney compared to their HRWI counterparts. Increased water reabsorption will reduce the amount of water consumed to attain hydration. The water reabsorption potential was reflected in the excreta moisture levels as the LRWI birds had significantly lower excreta moisture than the HRWI birds. Excreta moisture level require further studies and could be considered as a potential proxy trait for water intake.

Early pregnancy exposure of maternal triglyceride levels and its effects on birth weight.

OBJECTIVES: The aim of this study was to evaluate the early pregnancy exposure of maternal triglyceride (mTG) and its effects on birth weight, which was an important indicator for nutritional status of newborns, and even its long-term health. METHODS: A retrospective cohort study was designed to investigate the relationship between mTG in early pregnancy and birth weight. Totally 32,982 women who had a singleton pregnancy and underwent serum lipids screening during early pregnancy were included in this study. Logistic regressions were used to evaluate the correlations between mTG levels and small for gestational age (SGA) or large for gestational age (LGA), and the restricted cubic spline models were applied to explore the dose-response relationship. RESULTS: The increased mTG levels during early pregnancy decreased the risk of SGA and increased the risk of LGA. The high mTG (>90th, 2.05 mM) was showed associated with higher risk of LGA (AOR, 1.35; 95 %CI, 1.20 to 1.50), and lower risk of SGA (AOR, 0.78; 0.68 to 0.89). Lower risk of LGA (AOR, 0.81; 0.70 to 0.92) was found in those cases of low mTG (<10th, 0.81 mM), but no correlation was found between low mTG levels and the risk of SGA. The results remained robust after excluding women with high or low body mass index (BMI) and pregnancy complications. CONCLUSIONS: This study suggested that early pregnancy exposure of mTG were related to the occurrence of SGA and LGA. mTG levels higher than 2.05 mM (>90th) were suggested to be avoid because of its risk for LGA, while mTG lower than 0.81 mM (<10th) showed its benefits for ideal birthweight range.

Sweet taste preference is associated with greater hypothalamic response to glucose and longitudinal weight gain.

The hypothalamus has an abundant expression of sweet taste receptors that play a role in glucose sensing and energy homeostasis. Evidence suggests that liking "sweets" can be associated with weight gain, but the relationship between sweet taste preference and hypothalamic regulation of appetite is unknown. This study tested the hypothesis that sweet taste preference is associated with increased hypothalamic activation in response to glucose (a purported neural marker for weight gain risk) and greater longitudinal increases in body mass index (BMI). Fifty-four adults aged 18-35 years with a mean (± SD) BMI of 27.99 ± 5.32 kg/m2 completed the study. Height and weight were measured at baseline and 6-12 months later in a subset of 36 participants. Sweet taste preference was assessed via the Monell 2-series, forced-choice tracking procedure. Arterial spin labeling magnetic resonance imaging was performed before and after oral glucose ingestion to determine hypothalamic blood flow response to glucose. Linear models were used to examine relationships between sweet taste preference and the hypothalamic response to glucose and longitudinal changes in BMI, adjusting for age, sex, and baseline BMI. Sweet taste preference was positively associated with glucose-linked hypothalamic blood flow (beta = 0.017, p = 0.043), adjusted for age, sex and BMI. We also observed a positive association between sweet taste preference and longitudinal change in BMI (beta = 0.088, p = 0.015), adjusted for age, sex and baseline BMI. These findings suggest that heightened sweet taste preference is associated with glucose-linked hypothalamic activation and may be linked to increased susceptibility for weight gain.

Physiological protection against weight gain: evidence from overfeeding studies and future directions.

Body weight is under physiological regulation. When body fat mass decreases, a series of responses are triggered to promote weight regain by increasing food intake and decreasing energy expenditure. Analogous, in response to experimental overfeeding, excessive weight gain is counteracted by a reduction in food intake and possibly by an increase in energy expenditure. While low blood leptin and other hormones defend against weight loss, the signals that oppose overfeeding-induced fat mass expansion are still unknown. In this article, we discuss insights gained from overfeeding interventions in humans and intragastric overfeeding studies in rodents. We summarize the knowledge on the relative contributions of energy intake, energy expenditure and energy excretion to the physiological defence against overfeeding-induced weight gain. Furthermore, we explore literature supporting the existence of unidentified endocrine and non-endocrine pathways that defend against weight gain. Finally, we discuss the physiological drivers of constitutional thinness and suggest that overfeeding of individuals with constitutional thinness represents a gateway to understand the physiology of weight gain resistance in humans. Experimental overfeeding, combined with modern multi-omics techniques, has the potential to unveil the long-sought signalling pathways that protect against weight gain. Discovering these mechanisms could give rise to new treatments for obesity. This article is part of a discussion meeting issue 'Causes of obesity: theories, conjectures and evidence (Part I)'.

Hypothalamic DNA 5-hydroxymethylation levels are altered by diet-induced weight gain during the development of obesity in a sex-specific manner.

Obesity is a major health concern that is associated with altered gene transcription in the hypothalamus. However, the mechanisms controlling this gene expression dysregulation remain largely unknown. DNA 5-hydroxymethylation (5-hmC) is a potent transcriptional activator that is expressed at 10 times higher levels in the brain than the periphery. Despite this, no study has examined if DNA 5-hmC is altered in the brain following exposure to obesogenic diets or contributes to abnormal weight gain over time. Here, we used a rodent diet-induced obesity model in combination with quantitative molecular assays and CRISPR-dCas9 manipulations to test the role of hypothalamic DNA 5-hmC in abnormal weight gain in male and female rats. We found that males, but not females, have decreased levels of DNA 5-hmC in the hypothalamus following exposure to a high fat diet, which directly correlate with increased body weight. Short-term exposure to a high fat diet, which does not result in significant weight gain, resulted in decreased hypothalamic DNA 5-hmC levels, suggesting these changes occur prior to obesity development. Moreover, decreases in DNA 5-hmC persist even after the high fat diet is removed, though the extent of this is diet-dependent. Importantly, CRISPR-dCas9-mediated upregulation of DNA 5-hmC enzymes in the male, but not female, ventromedial nucleus of the hypothalamus significantly reduced the percentage of weight gained on the high fat diet relative to controls. These results suggest that hypothalamic DNA 5-hmC is an important sex-specific regulator of abnormal weight gain following exposure to high fat diets.

Artificial shade as a heat abatement strategy to grazing beef cow-calf pairs in a subtropical climate.

Grazing livestock in subtropical and tropical regions are susceptible to prolonged exposition to periods of extreme environmental conditions (i.e., temperature and humidity) that can trigger heat stress (HS). Currently, there is limited information on the effects of HS in the cow-calf sector globally, including in the southern U.S., as well as on mitigation strategies that could be implemented to improve animal well-being and performance. This study evaluated the impact of artificial shade (SHADE vs. NO SHADE) and breed (ANGUS vs. BRANGUS) on performance of pregnant-lactating cows, nursing heifers, and their subsequent offspring. Twenty-four Angus and 24 Brangus black-hided cows [579 ± 8 kg body weight (BW); approximately 85 d of gestation] and their nursing heifers (approximately 174 d of age) were randomly allocated to 12 'Pensacola' bahiagrass pastures (Paspalum notatum Flüggé; 1.3 ha, n = 4 pairs/pasture), with or without access to artificial shade [NO SHADE BRANGUS (NSB), NO SHADE ANGUS (NSA), SHADE BRANGUS (SB), and SHADE ANGUS (SA)] for 56 d that anticipated weaning during the summer season in Florida. Body condition score (BCS) of cows, blood samples, and BW of cow-calf pairs were obtained every 14 d during the 56-d experimental period until weaning. Following weaning (d 56), treatments were ceased, and cows and weaned heifers were managed alike. Weaned heifers were randomly allocated to 4 pens (n = 12/pen) equipped with GrowSafe feed bunks for 14 d to assess stress responses during weaning via plasma haptoglobin. An effect of SHADE × BREED interaction was detected for cow ADG, BW change, final BW, and final BCS, where SB had the greatest ADG, BW change, final BW, and final BCS. On d 14, SA cows had the greatest concentrations of insulin whereas on d 28 NSB had the lowest concentrations, NSA the greatest, and SA and SB being intermediate. On d 56, SA tended to have the greatest plasma insulin concentrations and SB the lowest. Weight gain per area (kg/ha) tended to be 11.4 kg/ha greater in SHADE vs. NO SHADE pastures. Pre-weaning calf ADG tended to be 0.14 kg greater for SHADE vs. NO SHADE calves. Weaning weight and BW at 14-d post-weaning were lesser for NSB vs. NSA, SA, and SB, whereas no differences in postweaning ADG or haptoglobin were observed. Effects of SHADE × BREED × day interaction was detected on plasma concentrations of IGF-1, in which NSA heifers had the lowest concentrations on weaning day. Gestation length was greater for SHADE vs. NO SHADE cows, but with no impacts on subsequent calf birth and weaning weight. In summary, providing artificial shade to pregnant-lactating beef cows increased body weight gain of nursing heifers and Brangus cows, while no impact on Angus dams were observed. The provision of artificial shade during the first trimester of gestation did not alter growth performance of the subsequent offspring at birth and weaning even though gestation length was longer.

Weight Gain in Early Infancy Impacts Appetite Regulation in the First Year of Life. A Prospective Study of Infants Living in Cyprus.

BACKGROUND: Eating behavior is associated with weight gain in infancy and childhood. Few studies found a bidirectional association between weight gain and eating behavior development in childhood, but there is little data on the association in early infancy, a period critical for the programming of obesity risk. OBJECTIVE: We investigated the bidirectional association between appetite traits and weight gain during the first year of life. METHODS: Participants were part of a cohort of 432 infants born in Cyprus. Appetite traits were measured using the Baby Eating Behavior Questionnaire or the Child Eating Behavior Questionnaire at age 2 to 4 wk, 6 mo, and 12 mo. Weight and length were collected at birth, 4 wk, 6 mo, and 12 mo. Multivariable linear regression was used to analyze associations between appetite traits at 2 to 4 wk and 6 mo and weight for age z-score change (WFAZC) between 4 wk and 6 mo and 6 and 12 mo. Associations were also analyzed in the opposite direction, between WFAZC from birth to 4 wk, 4 wk to 6 mo, and 6 mo to 12 mo and appetite traits at 4 wk, 6 mo, and 12 mo. RESULTS: Satiety responsiveness (SR) at 2 to 4 wk was associated with lower WFAZC from 4 wk to 6 mo (ß: -0.17; 95% CI: -0.30, -0.04) and SR at age 6 mo was associated with lower WFAZC from 6 to 12 mo (ß: -0.09; 95% CI: -0.17, -0.02). WFAZC from 4 wk to 6 mo was associated with higher enjoyment of food at 12 mo (ß: 0.11; 95% CI: 0.01, 0.20), higher food responsiveness at 12 mo (ß: 0.17; 95% CI: 0.04, 0.30), and lower SR at both 6 mo (ß: -0.11; 95% CI: -0.21, -0.01) and 12 mo (ß: -0.14; 95% CI: -0.24, -0.03). CONCLUSIONS: We found a bidirectional association between weight gain and appetite traits in infancy, suggesting that the effect of postnatal weight gain on obesity development is partly mediated by programming of appetite traits.

Relation of Overweight/Obesity to Reward Region Response to Food Reward and the Moderating Effects of Parental History of Eating Pathology in Adolescent Females.

OBJECTIVE: To test whether overweight/obesity is associated with an elevated reward region response to milkshake cues and a low reward region response to milkshake receipt. To test whether the risk for eating pathology moderates the effects of weight status on the neural response to milkshake cues and milkshake receipt. METHOD: The current study used functional magnetic resonance imaging (fMRI) to examine the neuronal responses of female adolescents (n = 80; M age = 14.6 ± 0.9; M BMI = 21.9 ± 3.6; 41% with a biological parental history of eating pathology) during a food receipt paradigm. RESULTS: Females with overweight/obesity showed a greater ventromedial prefrontal cortex (vmPFC), and ventral anterior cingulate (ACC) response to milkshake cues and a greater ventral striatum, subgenual ACC, and dorsomedial prefrontal cortex response to milkshake receipt than those with a healthy weight. Females with overweight/obesity plus a parental history of eating pathology showed a greater vmPFC/medial orbitofrontal cortex response to milkshake cues than those without a parental history of eating pathology and those with a healthy weight. Females with overweight/obesity and without a parental history of eating pathology showed a greater thalamus and striatum response to milkshake receipt. CONCLUSIONS: Overweight/obesity is associated with an elevated reward region response to palatable food cues and food receipt. A risk for eating pathology enhances the reward region response to food cues in those with excess weight.

How to address weight regain after bariatric surgery in an individualized way.

Bariatric surgery is the most effective obesity treatment. As a chronic and progressive disease, weight loss response to surgery will vary individually. Thus, insufficient weight loss or regain can happen after surgery, but they lack a standard definition. There are different mechanisms underlying weight regain and/or insufficient weight loss, such as genetics, maladaptive eating behaviors, and the inadequate choice of index operations, among others. Patients with weight regain or insufficient weight loss should be submitted to an individualized and comprehensive evaluation by a multidisciplinary team. This may help identify the causes and direct the appropriate treatment individually. Options for patients with insufficient weight loss and/or weight regain following bariatric surgery include repair of postoperative complications, conversion into another operation, endoscopic therapies with inconsistent outcomes, and dietary/behavioral counseling. Revision and conversion surgeries have higher complication rates than primary operations. Although there is no standard pharmacological regimen for that indication, the new agents seem efficient and safe to promote the loss of the regained weight and even be adjunctive to selected patients before they reach the plateau. This review aims to summarize the knowledge of the best approach for patients with weight regain/insufficient weight loss and suggests an algorithm to customize the approach and therapeutic options after bariatric surgery.