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Background Although mortality due to critical illness has fallen over decades, the number of patients with long-term functional disabilities has increased, leading to impaired quality of life and significant healthcare costs. As an essential part of the multimodal interventions available to improve outcome of critical illness, optimal nutrition therapy should be provided during critical illness, after ICU discharge, and following hospital discharge. Methods This narrative review summarizes the latest scientific insights and guidelines on ICU nutrition delivery. Practical guidance is given to provide optimal nutrition therapy during the three phases of the patient journey. Results Based on recent literature and guidelines, gradual progression to caloric and protein targets during the initial phase of ICU stay is recommended. After this phase, full caloric dose can be provided, preferably based on indirect calorimetry. Phosphate should be monitored to detect refeeding hypophosphatemia, and when occurring, caloric restriction should be instituted. For proteins, at least 1.3 g of proteins/kg/day should be targeted after the initial phase. During the chronic ICU phase, and after ICU discharge, higher protein/caloric targets should be provided preferably combined with exercise. After ICU discharge, achieving protein targets is more difficult than reaching caloric goals, in particular after removal of the feeding tube. After hospital discharge, probably very high-dose protein and calorie feeding for prolonged duration is necessary to optimize the outcome. High-protein oral nutrition supplements are likely essential in this period. Several pharmacological options are available to combine with nutrition therapy to enhance the anabolic response and stimulate muscle protein synthesis. Conclusions During and after ICU care, optimal nutrition therapy is essential to improve the long-term outcome to reduce the likelihood of the patient to becoming a “victim” of critical illness. Frequently, nutrition targets are not achieved in any phase of recovery. Personalized nutrition therapy, while respecting different targets during the phases of the patient journey after critical illness, should be prescribed and monitored.

Inflammation plays a key role in the pathogenesis of obesity. Chronic overfeeding leads to macrophage infiltration in the adipose tissue, resulting in proinflammatory cytokine production. Both microbial and endogenous danger signals trigger assembly of the intracellular innate immune sensor Nlrp3, resulting in caspase-1 activation and production of proinflammatory cytokines IL-1β and IL-18. Here, we showed that mice deficient in Nlrp3, apoptosis-associated speck-like protein, and caspase-1 were resistant to the development of high-fat diet-induced obesity, which correlated with protection from obesity-induced insulin resistance. Furthermore, hepatic triglyceride content, adipocyte size, and macrophage infiltration in adipose tissue were all reduced in mice deficient in inflammasome components. Monocyte chemoattractant protein (MCP)-1 is a key molecule that mediates macrophage infiltration. Indeed, defective inflammasome activation was associated with reduced MCP-1 production in adipose tissue. Furthermore, plasma leptin and resistin that affect energy use and insulin sensitivity were also changed by inflammasome-deficiency. Detailed metabolic and molecular phenotyping demonstrated that the inflammasome controls energy expenditure and adipogenic gene expression during chronic overfeeding. These findings reveal a critical function of the inflammasome in obesity and insulin resistance, and suggest inhibition of the inflammasome as a potential therapeutic strategy.

Exercise counteracts obesity effects, but information on how early-life obesity may affect long-term adaptation to exercise is lacking. This study investigates the impact of early-life postnatal overfeeding (PO) on animals' adaptation to exercise. Only male Wistar rats were used. On postnatal day (PN) 30, rats from control (NL-9 pups) or PO (SL-3 pups) litters were separated into four groups: NL-sedentary (NL-Se), NL-exercised (NL-Ex), SL-sedentary (SL-Se), and SL-exercised (SL-Ex). Exercised groups performed moderate-intensity exercise, running on a treadmill, from PN30 to PN90. Further experiments were carried out between PN90 and PN92. PO promoted obesity in SL versus NL rats (P < 0.05). Exercise reduced body weight (P < 0.001), body fat (P < 0.01), and improved glucose homeostasis in SL-Ex versus SL-Se. SL-Ex presented lower VO2max (P < 0.01) and higher post-exercise LDH (P < 0.05) compared to NL-Ex rats. Although moderate exercise counteracted obesity in SL rats, early-life overnutrition restricts fitness gains in adulthood, indicating that early obesity may impair animals' adaptation to exercise.

Body fat distribution is an important predictor of the metabolic consequences of obesity, but the cellular mechanisms regulating regional fat accumulation are unknown. We assessed the changes in adipocyte size (photomicrographs) and number in response to overfeeding in upper- and lower-body s.c. fat depots of 28 healthy, normal weight adults (15 men) age 29 ± 2 y. We analyzed how these changes relate to regional fat gain (dual energy X-ray absorptiometry and computed tomography) and baseline preadipocyte proliferation, differentiation [peroxisome proliferator-activated receptor-γ2 (PPARγ2) and CCAAT/enhancer binding protein-α (C/EBPα) mRNA]), and apoptotic response to TNF-α. Fat mass increased by 1.9 ± 0.2 kg in the upper body and 1.6 ± 0.1 kg in the lower body. Average abdominal s.c. adipocyte size increased by 0.16 ± 0.06 μg lipid per cell and correlated with relative upper-body fat gain (r = 0.74, P < 0.0001). However, lower-body fat responded to overfeeding by fat-cell hyperplasia, with adipocyte number increasing by 2.6 ± 0.9 × 10⁹ cells (P < 0.01). We found no depot-differences in preadipocyte replication or apoptosis that would explain lower-body adipocyte hyperplasia and abdominal s.c. adipocyte hypertrophy. However, baseline PPARγ2 and C/EBPα mRNA were higher in abdominal than femoral s.c. preadipocytes (P < 0.005 and P < 0.03, respectively), consistent with the ability of abdominal s.c. adipocytes to achieve a larger size. Inherent differences in preadipocyte cell dynamics may contribute to the distinct responses of different fat depots to overfeeding, and fat-cell number increases in certain depots in adults after only 8 wk of increased food intake.

•Epicardial adipose tissue has unique anatomic, biomolecular, and genetic features.•Epicardial fat transcriptome and secretome regulate myocardial thermogenesis, lipid, and glucose metabolism•A disequilibrium between epicardial fat feeding and overfeeding the myocardium leads to intramyocardial fat infiltration causing organ damage and clinical consequences.•The upregulation of epicardial fat pro-inflammatory, lipogenic and dysglycemic genes contributes to the fat build up in the proximal coronary arteries.•Epicardial fat is a measurable and modifiable risk factor that can serve as a novel diagnostic marker and therapeutic target. Epicardial adipose tissue is a particular visceral fat depot with unique anatomic, biomolecular, and genetic features. Epicardial fat displays both physiological and pathological properties. Epicardial fat expresses genes and secretes cytokines actively involved in the thermogenesis and regulation of lipid and glucose metabolism of the adjacent myocardium. A disequilibrium between epicardial fat feeding and overfeeding the myocardium with free fatty acids leads to intramyocardial fat infiltration causing organ damage and clinical consequences. The upregulation of epicardial fat proinflammatory and lipogenic genes contributes to the fat build up in the proximal coronary arteries. Epicardial fat is a measurable and modifiable risk factor that can serve as a novel and additional tool for cardiovascular risk stratification. Pharmacologically targeting epicardial fat with drugs such as glucagon peptide-like 1 analogs or sodium glucose transport 2 inhibitors reduces the epicardial fat burden and induces beneficial cardiometabolic effects. Assessment and manipulation of epicardial fat transcriptome might open new avenues in the prevention of cardiometabolic diseases.

The purpose of the present study was to determine whether probiotic supplementation (Lactobacillus casei Shirota (LcS)) prevents diet-induced insulin resistance in human subjects. A total of seventeen healthy subjects were randomised to either a probiotic (n 8) or a control (n 9) group. The probiotic group consumed a LcS-fermented milk drink twice daily for 4 weeks, whereas the control group received no supplementation. Subjects maintained their normal diet for the first 3 weeks of the study, after which they consumed a high-fat (65 % of energy), high-energy (50 % increase in energy intake) diet for 7 d. Whole-body insulin sensitivity was assessed by an oral glucose tolerance test conducted before and after overfeeding. Body mass increased by 0·6 (se 0·2) kg in the control group (P< 0·05) and by 0·3 (se 0·2) kg in the probiotic group (P>0·05). Fasting plasma glucose concentrations increased following 7 d of overeating (control group: 5·3 (se 0·1) v. 5·6 (se 0·2) mmol/l before and after overfeeding, respectively, P< 0·05), whereas fasting serum insulin concentrations were maintained in both groups. Glucose AUC values increased by 10 % (from 817 (se 45) to 899 (se 39) mmol/l per 120 min, P< 0·05) and whole-body insulin sensitivity decreased by 27 % (from 5·3 (se 1·4) to 3·9 (se 0·9), P< 0·05) in the control group, whereas normal insulin sensitivity was maintained in the probiotic group (4·4 (se 0·8) and 4·5 (se 0·9) before and after overeating, respectively (P>0·05). These results suggest that probiotic supplementation may be useful in the prevention of diet-induced metabolic diseases such as type 2 diabetes.

BACKGROUND: The current literature on the influences of family environment on childhood obesity is predominantly based on western populations and has focused on the role of parents. This study examined the influence of grandparents on the development of obesity among Chinese primary school aged children. METHODS: A mixed methods study was conducted in four socioeconomically distinct primary school communities in two cities of southern China. The qualitative study (17 focus groups and four personal interviews) involved parents, grandparents, school staff, and food retailers in the vicinity of the schools (n = 99) and explored perceived causes of childhood obesity. The cross-sectional study examined the association between children’s objectively measured weight status and reported health behaviours, and the presence and role of grandparents in the household. It included children from three randomly selected third grade (8 to 10 years) classes from each school (n = 497). RESULTS: Grandparents were commonly perceived to contribute to childhood obesity through inappropriate perception (e.g. fat children are healthy and well cared for), knowledge (e.g. obesity related diseases can only happen in adults; the higher the dietary energy/fat content, the more nutritious the food), and behaviour (e.g. overfeeding and indulging through excusing the children from household chores). Conflicting child care beliefs and practices between grandparents and parents, and between grandparents and school teachers, were felt to undermine efforts to promote healthy behaviours in children. In the cross-sectional study, children who were mainly cared for by their grandparents were more likely to be overweight/obese (adjusted OR = 2.03; 95 % CI = 1.19 to 3.47); and to consume more sugar-added drinks and unhealthy snacks (B = 2.13, 95 % CI = 0.87 to 3.40), than children who were mainly cared for by their parents or other adult. Children who lived with two or more grandparents in the household were more likely to be overweight/obese than children who did not live with any grandparent (adjusted OR = 1.72; 95 % CI = 1.00 to 2.94). CONCLUSIONS: Involvement of grandparents in childcare is an important factor contributing to childhood obesity in China. Future preventive interventions should include strategies that target grandparents.

Polycystic ovary syndrome (PCOS) is a well-known reproductive syndrome usually associated with obesity, insulin resistance, and hyperinsulinemia. Although the first signs of PCOS begin early in adolescence, it is underexplored whether peripubertal obesity predisposes women to PCOS metabolic disturbances. To highlight that, we examined the impact of postnatal overfeeding-induced obesity, achieved by litter size reduction during the suckling period, on metabolic disturbances associated with visceral and subcutaneous adipose tissue (VAT and SAT) function in the 5α-dihydrotestosterone (5α-DHT)-induced animal model of PCOS. We analyzed markers of insulin signaling, lipid metabolism, and energy sensing in the VAT and SAT. Our results showed that postnatally overfed DHT-treated Wistar rats had increased VAT mass with hypertrophic adipocytes, together with hyperinsulinemia and increased HOMA index. In the VAT of these animals, insulin signaling remained unchanged while lipogenic markers decreased, which was accompanied by increased AMPK activation. In the SAT of the same animals, markers of lipogenesis and lipolysis increased, while the activity of AMPK decreased. Taken together, obtained results showed that postnatal overfeeding predisposes development of PCOS systemic insulin resistance, most likely as a result of worsened metabolic function of SAT, while VAT preserved its tissue insulin sensitivity through increased activity of AMPK.

Background Postnatal overfeeding activates tissue glucocorticoid (GC) activity by up-regulating 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) and increasing sensitivity to high-fat (HF) diet-induced non-alcoholic fatty liver disease (NAFLD). The present study aimed to evaluate the effects of postnatal overfeeding on GC regulation and lipogenesis in the liver and to observe the impact of GC on hepatocyte lipid metabolism. Methods In vivo , Male Sprague-Dawley rat pup litters were adjusted to litter sizes of three (small litter, SL) or ten (normal litter, NL) on postnatal day 3 and then given standard chow from postnatal week 3 (W3) to W13. In vitro , HepG2 cells were stimulated by GC, mifepristone (Mi) or GC + Mi within 48 h, followed by sodium oleate (OA) intervention (or not) for 24 h. Intracellular lipid droplets, triglyceride (TG) concentrations and gene expression related to lipid metabolism were measured in hepatic tissues or HepG2 cells. Results In vivo , weight gain in the body and liver and TG concentrations in the liver were significantly increased in the SL rats compared to the NL rats at W3 and W13 ( p  < 0.05); mRNA expression of hepatic 11β-HSD1, acetyl-CoA carboxylase 1 (ACC), stearoyl-CoA desaturase-1 (SCD1), fatty acid synthase (FASN) and their nuclear transcription factor, sterol regulatory element binding protein-1c (SREBP-1c) ( p  < 0.05), was also increased. In vitro, intracellular lipid droplets and TG content in HepG2 cells increased under stimulation with GC or OA ( p  < 0.05); the increase was more significant following treatment with GC and OA together ( p  < 0.05). The ACC, SCD1, FASN and SREBP-1c mRNA expression changes were highly similar to the changes in TG content in cells. All the changes induced by GC disappeared when the glucocorticoid receptor (GR) was blocked by Mi. Conclusions Postnatal overfeeding induced GC overexposure through 11β-HSD1 up-regulation in the liver. GC activated hepatic de novo lipogenesis (DNL) via GR and led to hepatic lipid accumulation, which increased the risk of NAFLD during adulthood.

Lion-head goose is a large-sized breed native to Guangdong Province, China, exhibits remarkable capacity for fatty liver production under overfeeding conditions and is highly valued by local farmers and consumers. However, the molecular mechanisms driving fatty liver development in this breed are still unknown. In this study, we evaluated liver weight differences between normally fed and overfed Lion-head geese and further examined sex-specific differences following overfeeding. Overfeeding significantly increased liver weight more than 340%, and males possess a stronger capacity for lipid deposition under the same feeding regimen compared with females. RNA-Seq analysis identified 1476 differentially expressed genes (DEGs) shared by both sexes, which were mainly enriched in lipid and energy metabolism, oxidative stress, and mitochondrial pathways. In addition, 627 male-specific and 420 female-specific DEGs revealed sex-dependent differences, with males showing stronger transcriptional regulation and females exhibiting enhanced antioxidant and detoxification responses. Weighted gene co-expression network analysis (WGCNA) revealed 320 co-hub genes enriched in lipid and energy metabolism in overfeeding-induced fatty liver, along with 9 co-hub genes related to sex differences. Alternative splicing (AS) analysis detected 131 differentially spliced genes (DSGs). Integration of both approaches identified 7 overlapping genes, HYCC2 (Hyccin PI4KA lipid kinase complex subunit 2), AGL (Amylo-Alpha-1,6-Glucosidase and 4-Alpha-Glucanotransferase), CCDC62 (Coiled-coil domain containing 62), IGSF5 (Immunoglobulin superfamily member 5), MGARP (Mitochondria-localized glutamic acid-rich protein), CD80 (Cluster of Differentiation 80), and FPGS (Folylpolyglutamate synthase), as potential key regulators. These findings provide new insights into transcriptional and post-transcriptional regulation of overfeeding-induced fatty liver in geese.