Onset Of Obesity Research Articles

Genome-wide association study based on clustering by obesity-related variables uncovers a genetic architecture of obesity in the Japanese and the UK populations

Whether all obesity-related variants contribute to the onset of obesity or one or a few variants cause obesity in genetically heterogeneous populations remains obscure. Here, we investigated the genetic architecture of obesity by clustering the Japanese and British populations with obesity using obesity-related factors. In Step-1, we conducted a genome-wide association study (GWAS) with body mass index (BMI) as the outcome for eligible participants. In Step-2, we assigned participants with obesity (BMI ≥25 kg/m2) to five clusters based on obesity-related factors. Subsequently, participants from each cluster and those with a BMI <25 kg/m2 were combined. A GWAS was conducted for each cluster.Several previously identified obesity-related genes were verified in Step-1. Of the genes detected in Step-1, unique obesity-related genes were detected separately for each cluster in Step-2. Our novel findings suggest that a smaller sample size with increased homogeneity may provide insights into the genetic architecture of obesity.

Effect of Obesity on Aquaporin5 Expression in Human Placental and Uterus Tissues.

Background: Obesity and overweight are also becoming more prevalent among women of childbearing age and pregnant women. In maternal obesity, the activation of metabolic, inflammatory, and oxidative stress pathways is proven, which appears to be a key step in the pathological changes observed in placental and uterine function. Several recent studies have evidenced that aquaporins (AQPs) are critical players in adipose tissue biology and are involved in the onset of obesity. Methods: Our studies aimed to investigate the changes in placental volume and vascularization and measure the AQP5 expression and total antioxidant capacity (TAC) in the placenta and uterus tissues in obese and typical-weight mothers. We also aim to measure the AQP5 plasma concentration. Results: We found AQP5 dominance in the uterus and plasma at 34 weeks of normal pregnancy. The placental volume increased and the vascularization decreased in obese mothers compared to the control. The AQP5 expression increased in the uterus of the obese group and did not change in the placenta. The TAC decreased in the plasma of overweight mothers. Conclusions: We hypothesize that increased AQP5 expression prolongs the length of pregnancy and inhibits the onset of contractions. Based on our findings, we can develop diagnostic tests and provide new targets for tocolytic drug development.

Undetected and undiagnosed comorbidity in patients with obesity undergoing bariatric surgery-Results from the Berlin Bariatric Cohort study.

The quality of general obesity management before bariatric surgery (BS) is rarely investigated. Inadequate information regarding undetected and undiagnosed comorbidities (UUCs) in individuals with obesity may influence the penetration, risks, and outcomes of BS. We conducted a cohort study involving a pre-specified medical check-up in a cooperation between a BS department and an outpatient medical centre. A total of 1068 patients (74.4% women) were enrolled in the study. The mean age was 42.1 years (standard deviation [SD] 11.9) and the mean body mass index (BMI) was 46.1 (SD 6.91). The onset of obesity occurred in 11.4% of patients during childhood, 47.2% during schooltime/adolescence, 41.4% in adulthood. Gender differences were observed: men had higher BMI, systolic blood pressure, and impaired metabolic state (including diabetes, dyslipidemia, and liver disease with p-values <.001 for all). Women had lower haemoglobin levels, impaired iron status, lower albumin levels (p < .001), and increased C-reactive protein levels (p < .05). The prevalence of UUC conditions (percentage of cases) was as follows: arterial hypertension, 53%; decreased cystatin C clearance, 57%; dyslipidemia, 41%; fatty liver, 40%; iron deficiency, 37%; diabetes mellitus, 34%; vitamin D deficiency, 32%; chronic pain syndrome, 23%; liver fibrosis, 12%; obstructive sleep apnea, 10%; and vitamin deficiencies (vitamin B12, folic acid, vitamin K1) <10%. Undiagnosed hypertension was more prevalent in younger women, and nutritional deficits were associated with high BMI in both genders. Older age and high BMI were associated with undiagnosed diabetes and decreased glomerular filtration rate in both genders, and with liver fibrosis in men. UUC are highly prevalent in individuals undergoing BS. A refined assessment is recommended to improve health conditions and outcome in these candidates.

Influence of α-lipoic acid on longevity and stress resistance in Drosophila melanogaster fed with a high-fat diet.

Consumption of a high-fat diet is accompanied by the risks of obesity and early onset of age-associated complications for which dietary interventions are imperative to combat. α-lipoic acid has been shown to hinder diet-induced obesity and induce lifespan-extending efficacy in model organisms. In this study, α-lipoic acid was investigated for its efficacy in improving lifespan and stress resistance in the Canton-S strain of Drosophila melanogaster fed with a high-fat diet. Furthermore, as mating status significantly impacts survival in fruit flies, flies were reared in two experimental groups-group one, in which males and females were bred together, and group two, in which males and females were bred separately. In group one, α-lipoic acid improved the mean lifespan, reduced the fecundity of females, and reduced the mean body weight of flies at a dose range of 2-2.5mM, respectively. In group two, α-lipoic acid improved the mean lifespan, reduced the fecundity of females, and reduced the mean body weight of flies at a dose range of 1-2.5mM, respectively. Improved climbing efficiency was observed with α-lipoic acid at the dose range of 1.5-2.5mM in flies of group one and 1-2.5mM in flies of group two, respectively. Administration of α-lipoic acid improved resistance to oxidative stress in only female flies of group one at 2.5mM, whereas in group two, both male and female flies exhibited enhanced resistance to oxidative stress with α-lipoic acid at a dose range of 2-2.5mM, respectively. Male and female flies of only group one showed improved resistance to heat shock stress with α-lipoic acid at a dose range of 2-2.5mM. Only female flies of group two exhibited a slight improvement in recovery time following cold shock with α-lipoic acid only at 2.5mM. No significant change in resistance to starvation stress was observed with any dose of α-lipoic acid in either group of flies. To summarize, data from this study suggested a probable dose and gender-dependent efficacy of α-lipoic acid in flies fed with a high-fat diet, which was significantly influenced by the mating status of flies due to varied rearing conditions.

Age of obesity onset affects subcutaneous adipose tissue cellularity differently in the abdominal and femoral region.

We aimed to examine the effect of age of obesity onset, sex, and their interaction on abdominal and femoral subcutaneous adipose tissue (SAT) morphology (degree of adipocyte hyperplasia or hypertrophy). In this cross-sectional study, we isolated adipocytes via collagenase digestion from abdominal and femoral SAT biopsies taken from maleand femaleadults with childhood-onset obesity (CO; n = 8 males, n = 16 females) or adult-onset obesity (AO; n = 8 males, n = 13 females). Regional body composition was measured with dual-energy x-ray absorptiometry and a single-slice abdominal computed tomography scan. Mean adipocyte size was measured in abdominal and femoral SAT and was used to quantify morphology in android and gynoid subcutaneous fat, respectively. Abdominal SAT morphology was more hyperplastic in females with CO than females with AO (p = 0.004) but did not differ between males with CO and males with AO (p = 0.996). Conversely, femoral SAT morphology was more hypertrophic in males and females with CO than those with AO. Age of obesity onset appears to affect SAT morphology differently in the abdominal and femoral regions of male and female adults. Our findings challenge the notion that SAT is uniformly hyperplastic in CO and hypertrophic in AO.

Calorie Restriction Attenuates Memory Impairment and Reduces Neuroinflammation in Obese Aged Rats.

Obesity and aging collectively potentiate inflammatory responses, particularly within the central nervous system. Managing obesity presents a significant challenge, even more so considering the context of aging. Caloric restriction (CR) has been extensively documented in the literature for its multiple health benefits. Motivated by these findings, we hypothesized that CR could serve as a valuable intervention to address the brain alterations and cognitive decline associated with obesity in aged rats. Our investigation revealed that cafeteria diet increased hippocampal and hypothalamic transcripts related to neuroinflammation, along with cognitive deficits determined in the object recognition test in 18-month-old male rats. Western blot data indicate that the obesogenic diet may disrupt the blood-brain barrier and lead to an increase in Toll-like receptor 4 in the hippocampus, events that could contribute to the cognitive deficits observed. Implementing CR after the onset of obesity mitigated neuroinflammatory changes and cognitive impairments. We found that CR increases GABA levels in the hippocampus of aged animals, as demonstrated by liquid chromatography coupled with mass spectrometry analysis. These findings underscore the potential of CR as a therapeutic opportunity to ameliorate the neuroinflammatory and cognitive alterations of obesity, especially in the context of aging.

The infants' gut microbiome: setting the stage for the early onset of obesity.

In the past three decades, dietary and lifestyle changes worldwide have resulted in a global increase in the prevalence of obesity in both adults and children. Known to be highly influenced by genetic, environmental and lifestyle factors, obesity is characterized by a low-grade chronic inflammation that contributes to the development of other metabolic diseases such as diabetes and cardiovascular disease. Recently, the gut microbiome has been added as a cause/contributor to the development of obesity. As differences in the microbiome between obese and normoweight individuals have been observed, we set out to determine whether infants harbor an obesogenic microbiome early on and whether the pre-pregnancy status of the mother (obese or normoweight) is correlated to their infant's microbiome composition. Using shotgun sequencing, we analyzed stool samples throughout the first year of life from infants born to obese (n = 23 participants, m = 104 samples) and normoweight (n = 23 participants, m = 99 samples) mothers. We found that the infants' microbiome diversity at taxonomic and functional levels was significantly influenced by time (ANOVA p < 0.001) but not by the mother's pre-pregnancy status. Overall, no deterministic succession of taxa or functions was observed. However, infants born to obese mothers were found to have a significantly higher Bacillota/Bacteroidota ratio (p = 0.02) at six months, were significantly depleted from six months old of the well-established obesity biomarkers Akkermansia municiphila and Faecalibacterium prausnitzii (p < 0.01), and were at one week old, significantly enriched in pathways such as the UDP-N-acetyl-D-glucosamine biosynthesis II (p = 0.02) involved in leptin production, suggesting perhaps that there may exist some underlying mechanisms that dictate the development of an obesogenic microbiota early on.

Duración de la lactancia materna y condición nutricional de los lactantes en España. Estudio LAyDI (PAPenRed)

IntroductionBreastfeeding appears to protect the onset of obesity in infants. The aim is to know whether breastfeeding duration of is associated with the risk of obesity in infants and toddlers aged 12 and 24 months. Material and methodsProspective longitudinal study in a cohort of children born in Spain between April 2017 and March 2018 (LAyDI study) in the paediatric primary care system conducted in the framework of the PAPenRed research network. Analysis of breastfeeding duration (group 1: fewer than 6 months; group 2: 6 months or more) and its association with anthropometric variables. ResultsA total of 1495 patients attended the 12 months preventive child health visit and 1073 patients the 24 months visit. We found a statistically significant association between breastfeeding duration and weight-for-age, BMI-for-age and weight-for-length/height at 12 and 24 months; breastfeeding duration of less than 6 months was significantly associated with overweight and obesity (based on BMI-for-age and weight-for-length/height) at ages 12 and 24 months. Maternal pre-pregnancy BMI acted as a modifier on the association between breastfeeding duration and overweight and obesity (based on BMI-for-age). ConclusionsA breastfeeding duration of less than 6 months is associated with a higher percentage of overweight and obesity at ages 12 and 24 months, although maternal pre-pregnancy BMI modifies this relationship at 24 months.

β-Glucan-based superabsorbent hydrogel acts as a gastrointestinal exoskeleton enhancing satiety and interfering fat hydrolysis

Fat and its hydrolysis products, fatty acids, are indispensable nutritional components; however, prolonged excessive fat consumption, particularly in western diets, contributes to the onset of obesity and multiple metabolic disorders. In this study, we propose a daily-ingestible hydrogel (denoted as βC-MA hydrogel) composed of natural β-glucan and sodium carboxymethylcellulose crosslinked by malic acid at 120 °C. This hydrogel exhibits rapid swelling performance, up to 24-fold within 1 min and 176-fold after 1 h in deionized water. It also lengthens gastric retention and increases endogenous satiety signal levels, potentially controlling appetite and reducing food intake. Furthermore, βC-MA hydrogels that enter the small intestine can effectively inhibit fat hydrolysis and decrease triglyceride synthesis and transport. Specifically, the hydrogels inhibit the release of free fatty acids (FFAs) by approximately 50 % during digestion, influence the translocation of triglycerides and FFAs across the intestinal epithelium, and reduce the serum triglyceride levels by 22.2 %. These findings suggest that βC-MA hydrogels could serve as a noninvasive gastrointestinal device for weight control, with the advantage of reducing food intake and restoring lipid metabolism homeostasis.

Shared Genetic Influences Between Loss-of-Control Eating and Body Mass Index in Adolescent Twins.

Pediatric loss-of-control (LOC) eating is associated with high BMI and predicts binge-eating disorder and obesity onset with age. Research on the etiology of this common comorbidity has not explored the potential for shared genetic risk. This study examined genetic and environmental influences on LOC eating and its shared influence with BMI. Participants were 499 monozygotic and 398 same-sex dizygotic twins (age = 17.38 years ± 0.67, BMIz = 0.03 ± 1.03, 54% female) from the Colorado Center for Antisocial Drug Dependence Study. LOC eating was assessed dichotomously. Self-reported height and weight were converted to BMIz. Univariate and bivariate twin models estimated genetic and environmental influences on LOC eating and BMIz. More girls (21%) than boys (9%, p < 0.001) reported LOC eating. The phenotypic correlation with BMIz was 0.03 in girls and 0.18 in boys. Due to the nonsignificant phenotypic correlation in girls, bivariate twin models were fit in boys only. Across all models, the best-fitting model included genetic and unique environmental effects. Genetic factors accounted for 0.51 (95% CI: 0.23, 0.73) of the variance of LOC eating in girls and 0.54 (0.18, 0.90) in boys. The genetic correlation between LOC eating and BMIz in boys was 0.45 (0.15, 0.75). Findings indicate moderate heritability of LOC eating in adolescence, while emphasizing the role of unique environmental factors. In boys, LOC eating and BMIz share a proportion of their genetic influences.

Osteoprotegerin mediates adipogenesis in obesity

IntroductionAdipogenesis, the process of white adipose tissue expansion, plays a critical role in the development of obesity. Osteoprotegerin (OPG), known for its role in bone metabolism regulation, emerges as a potential regulator in mediating adipogenesis during obesity onset. ObjectivesThis study aims to elucidate the involvement of OPG in adipogenesis during the early phases of diet-induced obesity and explore its therapeutic potential in obesity management. MethodsUsing a diet-induced obesity model, we investigated OPG expression patterns in adipocytes and explored the mechanisms underlying its involvement in adipogenesis. We also assessed the effects of targeted silencing of OPG and recombinant OPG administration on obesity progression and insulin resistance. Additionally, the impact of electroacupuncture treatment on OPG levels and obesity management was evaluated in both animal models and human participants. ResultsOPG expression was prominently activated in adipocytes of white adipose tissues during the early phase of diet-induced obesity. Hyperlipidemia induced Cbfa1-dependent OPG transcription, initiating and promoting adipogenesis, leading to cell-size expansion and lipid storage. Intracellular OPG physically bound to RAR and released the PPARɤ/RXR complex, activating adipogenesis-associated gene expression. Targeted silencing of OPG suppressed obesity development, while recombinant OPG administration promoted disease progression and insulin resistance in obese mice. Electroacupuncture treatment suppressed obesity development in an OPG-dependent manner and improved obesity parameters in obese human participants. ConclusionOPG emerges as a key regulator in mediating adipogenesis during obesity development. Targeting OPG holds promise for the prevention and treatment of obesity, as evidenced by the efficacy of electroacupuncture treatment in modulating OPG levels and managing obesity-related outcomes.

Reconsidering the role of depression and common psychiatric disorders as partners in the type 2 diabetes epidemic

Common psychiatric disorders (CPDs) and depression contribute significantly to the global epidemic of type 2 diabetes (T2D). We postulated a possible pathophysiological mechanism that through Bridge-Symptoms present in depression and CPDs, promotes the establishment of emotional eating, activation of the reward system, onset of overweight and obesity and, ultimately the increased risk of developing T2D. The plausibility of the proposed pathophysiological mechanism is supported by the mechanism of action of drugs such as naltrexone-bupropion currently approved for the treatment of both obesity/overweight with T2D and as separate active pharmaceutical ingredients in drug addiction, but also from initial evidence that is emerging regarding glucagon-like peptide 1 receptor agonists that appear to be effective in the treatment of drug addiction. We hope that our hypothesis may be useful in interpreting the higher prevalence of CPDs and depression in patients with T2D compared with the general population and may help refine the integrated psychiatric-diabetic therapy approach to improve the treatment and or remission of T2D.

The age of the obesity onset is a very important factor for the development of metabolic complications and cardiovascular risk in children and adolescents with severe obesity

Severe obesity defined as BMI value corresponding to an adult > 40 kg/m2 affects 1–5% of children and adolescents in Europe. The purpose of this study was to assess the occurrence of cardiovascular risk factors in children and adolescents with severe obesity. The analysis included 140 patients (75 female) at the mean age of 14 ± 2.1 SD (range 10–18) years (all recruited in 4 regional reference centers in Poland). Severe obesity was defined as BMI > 35 kg/m2 (children 6–14 years), and BMI > 40 kg/m2 (> 14 years). Fasting plasma samples have been obtained in all patients, and OGTT was performed in all patients. The metabolic risk factors were defined as high blood pressure (BP > 90 percentile for height, age, and sex), HDL cholesterol < 1.03 mmol/L, TG ≥ 1.7 mmol/L, and hyperglycemic state (fasting blood glucose > 5.6 mmol/L, or blood glucose 120′ after oral glucose load > 7.8 mmol/L). Additionally, the MetS z-score was calculated using Metabolic Syndrome Severity Calculator. One hundred twenty-four (89%) participants presented with high BP, 117 (84%) with abnormal lipid profile, and 26 with the hyperglycemic. Only 12 (9%) were free of metabolic complications. More than 60% of patients had more than one cardiovascular risk factor. The high BP was significantly associated with the severity of obesity (F = 9.9, p = 0.002). Patients with at least one metabolic complication presented with significantly younger age of the onset of obesity (the mean age of the patients with no overt obesity complications was 10 years, while the mean age of those who presented at least one was 4.7 ± 3.5 SD years (p = 0.002)). A significant positive association between in the value of the Mets BMI z-score with age was observed (R = 0.2, p < 0.05). There were no differences between girls and boys regarding Mets BMI z-score (1.7 ± 0.8 vs 1.7 ± 0.7, p = 0.8).Conclusions: The most common metabolic risk factor in children and adolescents with severe obesity was high BP. The most important factor determining presence of obesity complications, and thus the total metabolic risk, seems to be younger (< 5 years) age of onset of obesity.What is Known?• It is estimated that 1-5% of children and adolescents in Europe suffer from severe obesity corresponding to an adult BMI > 40 kg/m2, and it is the fastest growing subcategory of childhood obesity.• Children with severe obesity face substantial health risk that may persist into adulthood, encompassing chronic conditions, psychological disorders and premature mortality.What is new:• The most common complication is high BP that is significantly associated with the severity of obesity (BMI z-score), contrary to dyslipidemia and hyperglycemic state, which do not depend on BMI z-score value.• The most important factor determining presence of obesity complications, and thus the total metabolic risk, seems to be younger (< 5 years) age of onset of obesity.

Association of parental obesity with the profile of metabolic-bariatric surgery patients: a cohort study of the German StuDoQ|MBE registry

ObjectivesTo investigate the association of parental obesity (PO) with onset of obesity, pre-surgical disease duration and body mass index (BMI) at the time of surgery in patients undergoing metabolic-bariatric surgery...

An autopsy case of an adult woman with Rapid-Onset Obesity with Hypoventilation, Hypothalamic, Autonomic Dysregulation, and Neuroendocrine Tumors (ROHHAD(NET)) syndrome developing nonalcoholic steatohepatitis and hepatocellular carcinoma: A case report.

Nonalcoholic steatohepatitis (NASH) is an important etiology of hepatocellular carcinoma (HCC), and there is no established therapy for this syndrome. Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, autonomic dysregulation, and neural crest tumor (ROHHAD(NET)) is an extremely rare syndrome considered to be life-threatening, with death occurring around 10 years of age. We present the oldest known autopsy case of this syndrome that developed HCC. This case provided important information on not only improving the course of this syndrome, but also understanding the natural history and therapeutic modalities of NASH and HCC. The patient was diagnosed with ROHHAD(NET) syndrome in childhood, and liver cirrhosis due to NASH was diagnosed at age 17. HCC was detected at age 20, and embolization and irradiation were performed. At age 21, she died from accidental acute pancreatitis and subsequent liver failure and pulmonary hemorrhage. Rapid onset of obesity, hypoventilation, and hypothalamic disturbance appeared in childhood and was diagnosed as this syndrome. At age 17, liver cirrhosis due to NASH was diagnosed by liver biopsy, and at age 20, HCC was diagnosed by imaging. Transarterial chemoembolization and irradiation were performed, and the HCC was well controlled for a year. At age 21, she died from accidental acute pancreatitis, subsequent liver failure and pulmonary hemorrhage. Autopsy revealed that the HCC was mostly necrotized. This case was valuable not only for other ROHHAD(NET) syndrome cases, but also in improving our understanding of the natural history of NASH and HCC.

Poor sleep quality and overweight/obesity in healthcare professionals: a cross-sectional study.

This study aimed to analyze the relationship between the sleep quality of healthcare professionals and the incidence of overweight and obesity, exploring the potential impact of sleep quality on the onset of overweight and obesity in order to provide a scientific basis for formulating effective health intervention measures. A convenience sampling method was used to conduct a survey on the sleep characteristics and obesity status among healthcare professionals at Peking Union Medical College Hospital and Tianjin Dongli District Traditional Chinese Medicine Hospital. The survey was conducted via online questionnaires, which included demographic data, the Pittsburgh Sleep Quality Index (PSQI), height, weight, and related sleep, exercise, and dietary habits. Univariate and multivariate logistic regression analyses were applied to study the relationship between sleep quality and overweight/obesity among healthcare professionals. A total of 402 questionnaires were distributed, with a 100% retrieval rate, yielding 402 valid questionnaires. The average body mass index of the 402 participants was 23.22 ± 3.87 kg/m^2. Among them, 144 cases were overweight or obese, accounting for 35.8% (144/402) of the total. The prevalence of poor sleep quality among healthcare professionals was 27.4% (110/402), with an average PSQI score of 8.37 ± 3.624. The rate of poor sleep quality was significantly higher in the overweight and obese group compared to the normal weight group (36.1% vs. 22.5%, p = 0.003). The multivariate analysis indicated that gender, marital status, lower education level, sleep duration (odds ratio [OR] =1.411, 95% confidence interval [CI] 1.043-1.910, p = 0.026), and sleep disturbances (OR = 1.574, 95%CI 1.123-2.206, p = 0.008) were significant risk factors for overweight and obesity among healthcare professionals. Overweight or obese healthcare professionals had poorer sleep quality compared to those with a normal weight. Sleep duration and sleep disorders were identified as independent risk factors for overweight or obesity in healthcare professionals. Increasing sleep duration and improving sleep disorders may play a positive role in controlling overweight and obesity among healthcare professionals.

Clinical phenotypes of adults with monogenic and syndromic genetic obesity.

Considering limited evidence on diagnostics of genetic obesity in adults, we evaluated phenotypes of adults with genetic obesity. Additionally, we assessed the applicability of Endocrine Society (ES) recommendations for genetic testing in pediatric obesity. We compared clinical features, including age of onset of obesity and appetite, between adults with non-syndromic monogenic obesity (MO), adults with syndromic obesity (SO), and adults with common obesity (CO) as control patients. A total of 79 adults with genetic obesity (32 with MO, 47 with SO) were compared with 186 control patientswith CO. Median BMI was similar among the groups: 41.2, 39.5, and 38.7 kg/m2 for patients with MO, SO, and CO, respectively. Median age of onset of obesity was 3 (IQR: 1-6) years in patients with MO, 9 (IQR: 4-13) years in patients with SO, and 21 (IQR: 13-33) years in patients with CO (p < 0.001). Patients with genetic obesity more often reported increased appetite: 65.6%, 68.1%, and 33.9% in patients with MO, SO, and CO, respectively (p < 0.001). Intellectual deficit and autism spectrum disorder were more prevalent in patients with SO (53.2% and 21.3%) compared with those with MO (3.1% and 6.3%) and CO (both 0.0%). The ES recommendations were fulfilled in 56.3%, 29.8%, and 2.7% of patients with MO, SO, and CO, respectively (p < 0.001). We found distinct phenotypes in adult genetic obesity. Additionally, we demonstrated low sensitivity for detecting genetic obesity in adults using pediatric ES recommendations, necessitating specific genetic testing recommendations in adult obesity care.

The impact of the obesity onset on the inflammatory and glycemic profile of women with severe obesity

BackgroundThe stage of life at the onset of obesity is an important factor in assessing inflammatory state and cardiometabolic risk. ObjectivesThis study aimed to evaluate the relationship between the obesity onset and the inflammatory profile in women with severe obesity. SettingPublic hospital, Brazil. MethodsForty-eight women with severe obesity (20–59 yr old) were evaluated according to weight, height, neck circumference (NC), waist circumference (WC), and hip circumference, as well blood metabolic and inflammatory parameters. The participants were grouped according to obesity onset stage of life (early group: ≤19 yr; late group: >19 yr). ResultsThe demographic means of the participants were: age of 39.7 years, weight of 122.7 kg and body mass index (BMI) of 48.4 kg/m2. The late group presented significantly higher values of leptin (lep)/adiponectin (adipo) ratio and homeostatic model assessment for insulin resistance (HOMA-IR) than the early group. The late group also had a lower adipo/lep ratio. Moreover, the late group showed correlations between the lep/adipo ratio and BMI (r = .460, P = .021), NC (r = .478, P = .016), and WC (r = .535, P = .006). Adipo was also correlated with NC (r = −.418, P = .038), WC (r = −.437, P = .029), and glycated hemoglobin (HbA1C) (r = −.485, P = .019). By contrast, in the early group, the lep/adipo ratio showed correlations with insulin (r = .647, P = .004) and HOMA-B (r = .564, P = .015). ConclusionsThe inflammatory profile is correlated with anthropometric values in women with late-onset obesity. Inflammatory markers seemed to correlate with the glycemic profile in women with early-onset obesity. Furthermore, inflammation was higher in women with late-onset obesity compared to those with early-onset obesity.

Fish oil supplementation during pregnancy decreases liver endocannabinoid system and lipogenic markers in newborn rats exposed to maternal high-fat diet.

Maternal high-fat diet (HF) programs obesity, metabolic dysfunction-associated steatotic liver disease (MASLD), hypertriglyceridemia, and hyperglycemia associated with increased endocannabinoid system (ECS) in the liver of adult male rat offspring. We hypothesized that maternal HF would induce sex specific ECS changes in the liver of newborn rats, prior to obesity onset, and maternal fish oil (FO) supplementation would reprogram the ECS and lipid metabolism markers preventing liver triglycerides (TG) accumulation. Female rats received a control (CT) (10.9% fat) or HF (28.7% fat) diet 8weeks prior to mating and during pregnancy. A subgroup of HF dams received 3% FO supplementation in the HF diet (35.4% fat) during pregnancy (HFFO). Serum hormones and liver TG, ECS, lipid metabolism, oxidative stress and autophagy markers were assessed in male and female newborn offspring. Maternal HF diet increased liver cannabinoid receptor 1 (CB1) in males and decreased CB2 in females, with no effect on liver TG. Maternal FO supplementation reduced liver CB1 regardless of the offspring sex, but reduced TG liver content only in females. FO reduced the liver content of the endocannabinoid anandamide in males, and the content of 2-arachidonoylglycerol in both sexes. Maternal HF increased lipogenic and decreased lipid oxidation markers, and FO induced the opposite regulation in the liver of offspring. Prenatal HF and FO differentially modulate liver ECS in the offspring before obesity and MASLD development. These results suggest that maternal nutrition at critical stages of development can modulate the offspring's ECS, predisposing or preventing the onset of metabolic diseases.

Trait food craving predicts functional connectivity between dopaminergic midbrain and the fusiform food area during eating imagery.

Neurofunctional coupling between the dopaminergic midbrain (i.e., ventral tegmental area, VTA) and higher-order visual regions may contribute to food craving, leading to the onset or maintenance of obesity. We recently showed that the VTA resting-state functional connectivity with the occipitotemporal cortex, at the level of the fusiform gyrus (FFG), was specifically associated with trait food craving and the implicit bias for food images, suggesting that VTA-FFG connectivity may reflect the association between the visual representations of food and its motivational properties. To further test this hypothesis, this time we studied task-based functional connectivity in twenty-eight healthy-weight participants while imagining eating their most liked high-calorie (HC) or least liked low-calorie food (LC) or drinking water (control condition). Trait food craving scores were used to predict changes in task-based functional connectivity of the VTA during imagery of HC compared to LC foods (relative to the control condition). Trait food craving was positively associated with the functional connectivity of the VTA with the left FFG: people with higher trait food craving scores show stronger VTA-FFG connectivity, specifically for the imagery of the liked HC foods. This association was not linked to the quality of imagery nor to state measures of craving, appetite, or thirst. These findings emphasize the contribution of the functional coupling between dopaminergic midbrain and higher-order visual regions to food craving, suggesting a neurofunctional mechanism by which the mental representations of the HC food we like can become much more salient if not irresistible.