Explore the vast range of titles available.

Ultrasound (US) provides the most accurate technique for thickness measurements of subcutaneous adipose tissue (SAT) layers. This US method was recently standardised using eight sites to capture SAT patterning and allows distinguishing between fat and embedded fibrous structures. These eight sites chosen for fat patterning studies do not represent the mean SAT thickness measured all over the body that is necessary for determining subcutaneous fat mass. This was obtained by SAT measurements at 216 sites distributed randomly all over the body. Ten participants with BMI below 28.5kgm −2 and SAT means (from eight sites) ranging from 3 mm to 10 mm were selected. The means from eight sites overestimated the means obtained from 216 sites (i.e. 2160 US measurements in the ten participants); the calibration factor of 0.65 corrects this; standard deviation (SD) was 0.05, i.e. 8%. The SD of the calibration factor transforms linearly when estimating the error range of the whole body’s SAT volume (body surface area times the calibrated mean SAT thickness). The SAT masses ranged from 3.2 to 12.4 kg in this group. The standard deviations resulting from solely the calibration factor uncertainty were ±0.3 and ±1.0 kg, respectively. For these examples, the SAT percentages were 4.9(±0.4)% and 13.3(±1.0)%.

Host responses to infection encompass many processes in addition to activation of the immune system, including metabolic adaptations, stress responses, tissue repair, and other reactions. The response to bacterial infection in Drosophila melanogaster has been classically described in studies that focused on the immune response elicited by a small set of largely avirulent microbes. Thus, we have surprisingly limited knowledge of responses to infection that are outside the canonical immune response, of how the response to pathogenic infection differs from that to avirulent bacteria, or even of how generic the response to various microbes is and what regulates that core response. In this study, we addressed these questions by profiling the D. melanogaster transcriptomic response to 10 bacteria that span the spectrum of virulence. We found that each bacterium triggers a unique transcriptional response, with distinct genes making up to one third of the response elicited by highly virulent bacteria. We also identified a core set of 252 genes that are differentially expressed in response to the majority of bacteria tested. Among these, we determined that the transcription factor CrebA is a novel regulator of infection tolerance. Knock-down of CrebA significantly increased mortality from microbial infection without any concomitant change in bacterial number. Upon infection, CrebA is upregulated by both the Toll and Imd pathways in the fat body, where it is required to induce the expression of secretory pathway genes. Loss of CrebA during infection triggered endoplasmic reticulum (ER) stress and activated the unfolded protein response (UPR), which contributed to infection-induced mortality. Altogether, our study reveals essential features of the response to bacterial infection and elucidates the function of a novel regulator of infection tolerance.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures ( P  < 5 × 10 −8 ). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms. Genome-wide association meta-analyses of waist-to-hip ratio adjusted for body mass index in more than 224,000 individuals identify 49 loci, 33 of which are new and many showing significant sexual dimorphism with a stronger effect in women; pathway analyses implicate adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution. Cardiometabolic traits linked to body fat distribution In the first of a pair of Articles in this issue from the GIANT Consortium, genome-wide association meta-analyses of waist and hip circumference-related traits in more than 200,000 individuals have been used to identify 49 loci — 33 of them new — associated with waist-to-hip ratio adjusted for body mass index and an additional 19 loci associated with related waist and hip circumference measures. A subset of these loci shows significant sexual dimorphism, with many showing a stronger effect in women. Analyses implicate adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms and offer potential targets for interventions in the risks associated with abdominal fat accumulation.

The mosquito fat body plays key roles in metabolism and immunity, yet its cellular diversity and specialization remain poorly understood. This study analyzed 97,650 nuclei from the female Anopheles gambiae abdominal body wall at single-nucleus resolution, identifying seven major cell types. Fat body trophocytes are most abundant ( ~ 85%), with five subpopulations: basal (T1, T2), metabolically enriched (T3), immune-responsive (T4), and a vitellogenic group (T5) found only in blood-fed females. Sessile hemocytes comprise 7.4% of cells and expression of lipid biosynthesis enzymes increase in oenocytes (1.1%) after immune priming. T4 trophocytes consistently express immune genes, while various cell types respond to bacterial infection. Blood feeding induces extensive transcriptomic changes, notably upregulating vitellogenin and DNA replication genes, indicating trophocyte endoreplication and metabolic shifts. Vitellogenin mRNA was expressed in the first layer of trophocytes facing the hemolymph with apical subcellular localization. This high-resolution atlas reveals specialized trophocyte roles in mosquito immunity and reproduction. The mosquito fat body plays key roles in metabolism and immunity. Here, using single-nuclei transcriptomics the authors reveal that blood feeding induces extensive transcriptomic changes, endoreplication and metabolic shifts in fat body trophocytes, while oenocytes respond to immune priming.

Background Parallel to growth of aging and obese populations, the prevalence of metabolic diseases is rising. How body mass index (BMI) relates to frailty and mortality across frailty levels is controversial. We examined the associations of high BMI with frailty and mortality and explored the effects of percent body fat on these associations. Methods We included 29,937 participants aged ≥50 years from the 2001–2006 National Health and Nutrition Examination Survey (NHANES) cohorts ( N =6062; 53.7% females) and from wave 1 (2004) of Survey of Health, Ageing and Retirement in Europe (SHARE) ( N =23,875; 54% females) . BMI levels were categorized as: normal: 18.5–24.9 kg/m 2 , overweight: 25.0–29.9, obese grade 1: 30.0–34.9, and obese grade 2 or 3: >35.0. A frailty index (FI) was constructed excluding nutrition-related items: 36 items for NHANES and 57 items for SHARE. We categorized the FI using 0.1-point increments: FI ≤ 0.1 (non-frail), 0.1 < FI ≤ 0.2 (very mildly frail), 0.2 < FI ≤ 0.3 (mildly frail), and FI > 0.3 (moderately/severely frail). Percent body fat was measured using DXA for NHANES participants. All-cause mortality data were obtained until 2015 for NHANES and 2017 for SHARE to estimate 10-year mortality risk. All analyses were adjusted for age, sex, educational, marital, employment, and smoking statuses. Results Mean age of participants was 63.3±10.2 years for NHANES and 65.0±10.0 years for SHARE. In both cohorts, BMI levels ≥25 kg/m 2 were associated with higher frailty, compared to normal BMI. In SHARE, having a BMI level greater than 35 kg/m 2 increased mortality risk in participants with FI≤0.1 (HR 1.31, 95%CI 1.02–1.69). Overweight participants with FI scores >0.3 were at lower risk for mortality compared to normal BMI [NHANES (0.79, 0.64–0.96); SHARE (0.71, 0.63–0.80)]. Higher percent body fat was associated with higher frailty. Percent body fat significantly mediated the relationship between BMI levels and frailty but did not mediate the relationship between BMI levels and mortality risk. Conclusions Being overweight or obese is associated with higher frailty levels. In this study, we found that being overweight is a protective factor of mortality in moderately/severely frail people and obesity grade 1 may be protective for mortality for people with at least a mild level of frailty. In contrast, obesity grades 2 and 3 may be associated with higher mortality risk in non-frail people. The relationship between BMI and frailty is partially explained by body fat.

Ag nanoparticles (AgNPs), a widely used non-antibiotic, antibacterial material, have shown toxic and other potentially harmful effects in mammals. However, the deleterious effects of AgNPs on insects are still unknown. Here, we studied the effects of AgNPs on the model invertebrate organism Bombyx mori . After feeding silkworm larvae different concentrations of AgNPs, we evaluated the changes of B. mori body weights, survival rates, and proteomic differences. The results showed that low concentrations (<400 mg/L) of AgNPs promoted the growth and cocoon weights of B. mori . Although high concentrations (≥800 mg/L) of AgNPs also improved B. mori growth, they resulted in silkworm death. An analysis of fat body proteomic differences revealed 13 significant differences in fat body protein spots, nine of which exhibited significantly downregulated expression, while four showed significantly upregulated expression. Reverse transcription–polymerase chain reaction results showed that at an AgNP concentration of 1600 mg/L, the expression levels of seven proteins were similar to the transcription levels of their corresponding genes. Our results suggest that AgNPs lowered the resistance to oxidative stress, affected cell apoptosis, and induced cell necrosis by regulating related protein metabolism and metabolic pathways in B. mori .

In Lepidoptera and Diptera, the fat body dissociates into single cells in nondiapause pupae, but it does not dissociate in diapause pupae until diapause termination. Using the cotton bollworm, Helicoverpa armigera, as a model of pupal diapause insects, we illustrated the catalytic mechanism and physiological importance of fat body cell dissociation in regulating pupal development and diapause. In nondiapause pupae, cathepsin L (CatL) activates matrix metalloproteinases (Mmps) that degrade extracellular matrix proteins and cause fat body cell dissociation. Mmp-induced fat body cell dissociation activates lipid metabolism through transcriptional regulation, and the resulting energetic supplies increase brain metabolic activity (i.e., mitochondria respiration and insulin signaling) and thus promote pupal development. In diapause pupae, low activities of CatL and Mmps prevent fat body cell dissociation and lipid metabolism from occurring, maintaining pupal diapause. Importantly, as demonstrated by chemical inhibitor treatments and CRISPR-mediated gene knockouts, Mmp inhibition delayed pupal development and moderately increased the incidence of pupal diapause, while Mmp stimulation promoted pupal development and moderately averted pupal diapause. This study advances our recent understanding of fat body biology and insect diapause regulation.

The honeybee ( Apis mellifera ) forms two female castes: the queen and the worker. This dimorphism depends not on genetic differences, but on ingestion of royal jelly, although the mechanism through which royal jelly regulates caste differentiation has long remained unknown. Here I show that a 57-kDa protein in royal jelly, previously designated as royalactin, induces the differentiation of honeybee larvae into queens. Royalactin increased body size and ovary development and shortened developmental time in honeybees. Surprisingly, it also showed similar effects in the fruitfly ( Drosophila melanogaster ). Mechanistic studies revealed that royalactin activated p70 S6 kinase, which was responsible for the increase of body size, increased the activity of mitogen-activated protein kinase, which was involved in the decreased developmental time, and increased the titre of juvenile hormone, an essential hormone for ovary development. Knockdown of epidermal growth factor receptor (Egfr) expression in the fat body of honeybees and fruitflies resulted in a defect of all phenotypes induced by royalactin, showing that Egfr mediates these actions. These findings indicate that a specific factor in royal jelly, royalactin, drives queen development through an Egfr-mediated signalling pathway. A queen among fruitflies The difference between the queen in a honeybee colony and the workers is not a matter of genetics but of nutrition: larvae that consume royal jelly become queens. The active royal-jelly ingredient has long remained elusive, but is now identified as royalactin, a previously known protein that exhibits epidermal growth factor (EGFR)-like effects on rat hepatocytes. Surprisingly, royalactin also induces queen-like phenotypes in the fruitfly Drosophila melanogaster , increasing body size and ovary development through an EGFR-mediated signalling pathway.

The current obesity epidemic poses a major public health issue since obesity predisposes towards several chronic diseases. BMI and total adiposity are positively correlated with cardiometabolic disease risk at the population level. However, body fat distribution and an impaired adipose tissue function, rather than total fat mass, better predict insulin resistance and related complications at the individual level. Adipose tissue dysfunction is determined by an impaired adipose tissue expandability, adipocyte hypertrophy, altered lipid metabolism, and local inflammation. Recent human studies suggest that adipose tissue oxygenation may be a key factor herein. A subgroup of obese individuals - the ‘metabolically healthy obese' (MHO) - have a better adipose tissue function, less ectopic fat storage, and are more insulin sensitive than obese metabolically unhealthy persons, emphasizing the central role of adipose tissue function in metabolic health. However, controversy has surrounded the idea that metabolically healthy obesity may be considered really healthy since MHO individuals are at increased (cardio)metabolic disease risk and may have a lower quality of life than normal weight subjects due to other comorbidities. Detailed metabolic phenotyping of obese persons will be invaluable in understanding the pathophysiology of metabolic disturbances, and is needed to identify high-risk individuals or subgroups, thereby paving the way for optimization of prevention and treatment strategies to combat cardiometabolic diseases.

Obesity is the most extended metabolic alteration worldwide increasing the risk for the development of cardiometabolic alterations such as type 2 diabetes, hypertension, and dyslipidemia. Body mass index (BMI) remains the most frequently used tool for classifying patients with obesity, but it does not accurately reflect body adiposity. In this document we review classical and new classification systems for phenotyping the obesities. Greater accuracy of and accessibility to body composition techniques at the same time as increased knowledge and use of cardiometabolic risk factors is leading to a more refined phenotyping of patients with obesity. It is time to incorporate these advances into routine clinical practice to better diagnose overweight and obesity, and to optimize the treatment of patients living with obesity.