Excessive Fat Deposition Research Articles

Dietary and nutrition considerations in caring for patients with nonalcoholic fatty liver disease: Updates for the practicing clinician.

Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease worldwide, affecting up to one-third of the global population. The disease is defined by excess fat deposition in the liver and has a strong correlation with metabolic syndrome, which, in turn, is also a risk factor for disease progression, including the development of steatohepatitis, advanced fibrosis, cirrhosis, and hepatocellular carcinoma. Although a number of medications are being explored for disease mitigation, nothing is currently approved, and the mainstay of therapy remains dietary and lifestyle intervention that promotes weight loss as well as management of comorbid conditions. The landscape that guides care for patients with NAFLD continues to evolve. Clinicians caring for these patients need to consider underlying disease state and nutrition risk in addition to concurrent related diagnoses, such as insulin resistance and hyperlipidemia, when formulating treatment plans. The following is a comprehensive review of the current dietary and nutrition considerations in the management of patients with NAFLD, with a special emphasis on implications for the practicing clinician.

Social Support and Mental Health among Obese and Non-obese

Context: Due to modernization, overeating becomes as trending topic due to its disturbance on our energy balance system and body weight. Behavioural issues such as overeating and sedentary lifestyle have impact on health through an increase in body mass index due to excessive deposition of body fat. Thus, it impacts on our body weight through positive energy balance in which there is an increase energy intake and decrease energy expenditure. On the other hand, it can be controlled through appropriate social support and optimum mental health. Aims: The objective of this study was to reveal predictor role of social support on mental health among obese and non-obese using regression analysis, to know mean difference in social support and mental health using Mann-Whitney test, and to identify the level of social support and mental health among obese and non-obese individuals. Methods and Material: The study design was non-experimental, quantitative study with descriptive in nature. The participants were 250 obese and 250 non-obese people and were collected from in Cuddalore district of Tamil Nadu, India. Both obese and non-obese participants were asked them to fill questionnaires with psychological tools namely the mental health inventory-38 (MHI-38) and multidimensional perceived social support scale (MDPSS). Results: The data distribution were in non-normal pattern and the statistical test used were non-parametric test. The results stated that the predictor variable social support has shown significant positive impact on mental health. The effect of social support over mental health was high among non-obese (R = .406, R2 = .168, adjusted R2=.164, co-efficient B = .667 and p = .000) than obese (R = .522, R2 = .272, adjusted R2 = .270, co-efficient B = .729 and p = .000). Social support and mental health have significant mean BMI difference among obese and non-obese in which obese people have higher social support and low mental health than non-obese people.

Hepatocyte Adenosine Kinase Promotes Excessive Fat Deposition and Liver Inflammation

Nonalcoholic fatty liver disease is highly associated with obesity and progresses to nonalcoholic steatohepatitis when the liver develops overt inflammatory damage. While removing adenosine in the purine salvage pathway, adenosine kinase (ADK) regulates methylation reactions. We aimed to study whether hepatocyte ADK functions as an obesogenic gene/enzyme to promote excessive fat deposition and liver inflammation. Liver sections of human subjects were examined for ADK expression using immunohistochemistry. Mice with hepatocyte-specific ADK disruption or overexpression were examined for hepatic fat deposition and inflammation. Liver lipidomics, hepatocyte RNA sequencing (RNA-seq), and single-cell RNA-seq for liver nonparenchymal cells were performed to analyze ADK regulation of hepatocyte metabolic responses and hepatocyte-nonparenchymal cells crosstalk. Whereas patients with nonalcoholic fatty liver disease had increased hepatic ADK levels, mice with hepatocyte-specific ADK disruption displayed decreased hepatic fat deposition on a chow diet and were protected from diet-induced excessive hepatic fat deposition and inflammation. In contrast, mice with hepatocyte-specific ADK overexpression displayed increased body weight and adiposity and elevated degrees of hepatic steatosis and inflammation compared with control mice. RNA-seq and epigenetic analyses indicated that ADK increased hepatic DNA methylation and decreased hepatic Ppara expression and fatty acid oxidation. Lipidomic and single-cell RNA-seq analyses indicated that ADK-driven hepatocyte factors, due to mitochondrial dysfunction, enhanced macrophage proinflammatory activation in manners involving increased expression of stimulator of interferon genes. Hepatocyte ADK functions to promote excessive fat deposition and liver inflammation through suppressing hepatocyte fatty acid oxidation and producing hepatocyte-derived proinflammatory mediators. Therefore, hepatocyte ADK is a therapeutic target for managing obesity and nonalcoholic fatty liver disease.

Body composition and its effects on Glucose metabolism in Obese and Nonobese adult males obesity and its effects on glucose and blood parameters

Background: Obesity is now considered as a global issue and its prevalence is increasing day by day especially in developed countries, it is a multifactorial medical condition in which excess fat deposition occurs in the body that causes detrimental effects to the health and leads person to a number of pathologies .Chronic obesity is associated with cardiovascular problems ,nonalcoholic fatty liver disease, impaired lipid metabolism and dysregulation in glucose metabolism in the body which itself is a door to many health consequences.Hba1c is a tool used to monitor average blood glucose levels of past 3 months and considered as one of the reliable tool for screening diabetes along with other protocols. This study is aimed to observe the effects of total body fat on the hba1c levels in normal ,non-diabetic and apparently healthy male adults Methodology :A case/control study was conducted between the duration of July 2020 to September 2020,total number of participants was n=118, data was collected from obese and non-obese participants, total body fat was obtained by BIA method ,anthropometric indices was recorded and blood was drawn for Hba1c test .Results: Among 118 individuals 70 (59.3%) were belong to age group 30-39 years and 48(40.7%) were belong to age group 40-49 years. Mean total body fat in normal group aged between 30-39 years is 14.7±3.1 and in the same group mean total body fat in obese is observed as 31.1±5.2, similarly in age group 40-49 years the mean TBF observed in nonobese is 15.3±2.6 whereas mean TBF in obese group is 30.6±5,In case of HbA1c 10(14.2%) participants in obese group of age group 30-39 shows HbA1c in pre diabetic range however 1(1.4%) participant in normal body composition shows prediabetic HbA1c, Whereas among participants of Age Group 40-49 13(27%) participants in obsess group and 02 (4.1%)among nonobese showed Hba1c in prediabetic range. Conclusion. Profound differences were observed in the glucose parameter of healthy obese and non- obese participants, people with more body fat showed derange HbA1c levels.

295 Effects of Prenatal Testosterone Excess on Puberty Attainment of First-Generation ewe Lambs

Abstract Prenatal testosterone excess causes reproductive perturbations in sheep that recapitulate those seen in women with polycystic ovary syndrome (PCOS). Obesity has a significant role in the development and severity of the PCOS phenotype. Our objective was to investigate the effects of testosterone excess from gestational days (GD) 60-90 (unlike the GD 30-90 model, these animals are not virilized) and postnatal body weight (BW) gain on puberty in first-generation ewe lambs. Pregnant Suffolk ewes received testosterone propionate (T; 100 mg) or corn oil (C) i.m. twice weekly from GD 60-90 (term=147d). Ewe lambs were weaned ~3 mo of age. Control and T lambs were assigned to gain either 0.3 kg/d (C and T-maintenance) or 0.4 kg/d (T-overfed). Maintenance diet was designed to promote optimal growth without excess fat deposition. Overfed ration was designed to achieve a BW ~30% above that of maintenance. Progesterone concentrations were measured via radioimmunoassay in blood samples collected twice weekly from ewe lambs (n=15/group) during the first breeding season. Puberty was defined as when progesterone concentrations were < 0.5 ng/mL for four consecutive samples followed by three consecutive samples ≥0.5 ng/mL. Six animals (C, n=1; T-maintenance, n=3; T-overfed, n=2) did not attain puberty during the study and puberty was assigned as last day of sampling. Average daily gain was not different among treatments (C, 0.23±0.02kg; T-maintenance, 0.25±0.01kg; T-overfed, 0.27±0.02kg). Age at puberty did not differ between groups (C, 274.6±9.9d; T-maintenance, 270.0±11.3d; T-overfed, 266.0±10.2d). Similarly, BW at puberty did not differ across treatments (C, 50.44±2.2kg; T-maintenance, 52.5±2.4kg; T-overfed, 57.3±2.5kg). In conclusion, unlike GD 30-90 exposure which advanced puberty, GD 60-90 exposure did not affect age and BW at puberty in ewe lambs. Collectively, these studies suggest that GD 30-60 is a critical developmental window in which prenatal testosterone excess advances puberty in female sheep. Research support: NIH-NICHD (R01HD099096).

Effect of High-Intensity Interval Training Combined with Blood Flow Restriction at Different Phases on Abdominal Visceral Fat among Obese Adults: A Randomized Controlled Trial.

Background: High-intensity interval training (HIIT) and blood flow restriction (BFR) represent a critical nonpharmacological strategy to reduce the excess deposition of visceral fat, as well as relevant complications, among obese populations. Applying BFR at diverse phases may have different effects. Therefore, the exercise program of this study combined HIIT with BFR, so as to explore the effect of BFR on abdominal visceral fat area and its mechanism in different periods of HIIT. The aim is to provide a more effective exercise prescription for obese people who want to reduce visceral fat quickly. Methods: This study was a randomized controlled trial involving 72 obese adults. One week before intervention, both regional and whole-body fat masses, abdominal subcutaneous and visceral fat areas, variables of blood metabolism, and VO2max were recorded. Additionally, subjects with a matched fat percentage were randomized as a no-training control (C), HIIT (H), HIIT with BFR during interval (I), and HIIT with BFR during exercise (E) groups for 24 sessions within a 12-week period, using a cycle ergometer. During session one, this study recorded blood lactate, specific serum lipolytic hormones, rating of perceived exertion (RPE), and exercise heart rate (HR) and compared them among three groups. The baseline tests were repeated at 1 week after intervention. Results: There was no significant statistical difference in the indicators of each group at baseline (p > 0.05). The improvement of trunk fat mass and fat percentage of the I and E groups markedly increased relative to the H group (p < 0.05). Meanwhile, the I group had improved android fat mass and whole-body fat mass relative to group H (p < 0.05). Those exercise groups had markedly improved indices compared with the C group (p < 0.05). Additionally, the reduction in the I group had remarkably superior abdominal visceral fat areas (AVFA) to the H and E groups (p < 0.05). Immediately and 30 min following exercise, the E and I groups had remarkably increased growth hormone (GH) compared with the H group (p < 0.05). After exercise, the I group showed markedly increased epinephrine (EPI) compared with the H group (p < 0.05). The LA level in the I group evidently increased relative to the E group (p < 0.05), while that in the E group evidently increased compared with the H group (p < 0.05). Conclusion: Compared with HIIT alone, HIIT with BFR can better improve the body-fat level and glucose metabolism. HIIT with BFR in the interval phase better reduces the abdominal visceral-fat level than in the exercise phase, which may be due to the increase in lipolytic hormone level caused by the higher physiological load.

Effects of metabolic energy intervention on lipid content and liver transcriptome in finisher yellow-feathered chickens

High-energy diets improve growth rates and shorten the growth period while resulting in excessive fat deposition in the liver of birds. The effect of different energy diets on lipid content and liver transcriptome in finisher Huxu chickens was examined here. A total of 200 90-d-old Huxu chickens with an average BW of 1.08 kg were randomly divided into two dietary treatments. The birds were fed diets either containing 12.06 MJ ME/kg (low metabolic energy, LME) or 13.31 MJ ME/kg (high metabolic energy, HME) for 45 days. Chickens fed the HME diet had significantly higher total triglyceride and total cholesterol concentrations in both plasma and liver than did those fed the LME diet. Transcriptomic profiling showed 480 known differentially expressed genes (DEG), with 180 down-regulated and 300 up-regulated chickens from the HME diet compared with the LME diet. Notably, these genes were mostly enriched in lipid metabolism including the PPAR signalling pathway, fatty acid elongation, and glycerophospholipid metabolism. The relative mRNA expression level of 14 lipid metabolism-related genes, included 13 up-regulated (MBOAT2, PLA2G2E, AGPAT2, AGPAT3, PCYT2, PEMT, ELOVL2, HADHA, ACOT1L, FABP3, FABP1, PLIN1, RXRG) and one down-regulated (LCAT) gene. In conclusion, the present findings indicate that a high-energy diet likely regulates gene expression of the 14 lipid metabolism-related genes through the PPAR signalling pathway, fatty acid elongation, and glycerophospholipid metabolism resulting in excessive fat accumulation in the liver of Huxu chickens. These results provide a better understanding of the biological mechanisms by which the increased dietary energy induces fat accumulation in the liver. Highlights A high-energy diet without change in protein level induced excessive fat accumulation in the Huxu chickens. Chickens fed the high-energy diet had induced higher total triglyceride and total cholesterol concentrations in both plasma and liver. This study showed a comprehensive profile of hepatic gene expression in chickens with fatty liver induced by high energy.

Visceral, subcutaneous, and total fat mass accumulation in a prospective cohort of adolescents

Race and sex differences in adolescents' body fat are demonstrated in cross-sectional cohorts, yet a longitudinal design would better identify patterns of fat distribution over time. The aim was to examine race and sex differences in adiposity between black and white adolescents over 2 y. A cohort of adolescents aged 10-16 y (38% black; 52% girls; 15% overweight, 34% with obesity) underwent body composition measurements at baseline (n = 309) and 2 y later (n = 236), using DXA to quantify whole-body fat mass (FM) and MRI for abdominal subcutaneous (SAT) and visceral adipose tissue (VAT) volumes. General linear models were used to examine race and sex differences in log-transformed FM, SAT, and VAT, adjusting for age, sexual maturation, extended BMI percentile, and race-by-sex interaction. SAT and VAT models in addition controlled for baseline FM and change in FM (for change models). Mean (95% CI) baseline FM (kg) was higher among white [18.5 (17.9, 19.2) than among black adolescents [17.4 (16.6, 18.2), P = 0.03] and girls [19.5 (18.8, 20.3) than boys [16.5 (15.8, 17.2), P < 0.0001]. Mean (95% CI) baseline SAT (L) was higher among girls [4.4 (4.2, 4.6)] than among boys [3.9 (3.7, 4.1), P < 0.0001]. Mean (95% CI) baseline VAT (L) was higher among white [0.5 (0.5, 0.6)] than among black [0.3 (0.3, 0.4)] adolescents (P < 0.0001) and boys [0.5 (0.4, 0.5)] than girls [0.4 (0.4, 0.4), P = 0.04]. Over 2 y mean (95% CI) FM change (kg) was higher among white [3.7 (2.9, 4.5)] than among black adolescents [2.3 (1.3, 3.3), P = 0.04] and girls [4.0 (3.0, 4.9)] than boys [2.0 (1.1, 3.0), P = 0.007], but SAT change (L) did not differ by race or sex. VAT change (L) was higher among white [0.1 (0.1, 0.1)] than among black adolescents [0.0 (0.0, 0.1), P = 0.003] and boys [0.1 (0.1, 0.1)] than girls [0.0 (0.0, 0.1), P = 0.034]. Sex and race differences in the deposition and accumulation of excess fat are important considerations for understanding obesity prevalence and obesity-related disease risk among adolescents.This trial was registered at clinicaltrials.gov as NCT02784509.

Ovine RAP1GAP and rBAT gene polymorphisms and their association with tail fat deposition in Hu sheep.

Excessive fat deposition in the tail of sheep will affect its feed efficiency, which will increase the feeding cost. The purpose of this study was to identify the single nucleotide polymorphisms (SNPs) of RAP1GAP and rBAT genes by PCR amplification and Sanger sequencing, the SNPs were genotyped by KASP genotyping assays to evaluate their association with tail fat deposition traits. The results showed that two intronic mutations of g.13561 G > A and g.1460 T > C were found in RAP1GAP and rBAT, respectively. There were three genotypes of GG, AG, AA and CC, CT and TT at these two loci, respectively. Association analysis showed that g.13561 G > A of RAP1GAP was associated with tail width, tail fat weight and relative tail fat weight (P < 0.05). The g.1460 T > C of rBAT was associated with tail width and tail fat weight (P < 0.05). Different combinations of genotypes also differed significantly with tail fat deposition traits. In the tail fat tissue, the expression levels of RAP1GAP gene was significantly higher in small-tailed sheep than in big-tailed sheep, and the expression levels of rBAT gene was significantly higher in big-tailed sheep than in small-tailed sheep. In the liver, the expression levels of RAP1GAP and rBAT gene was significantly higher at 6 months than at 0 and 3 months. In conclusion, RAP1GAP and rBAT polymorphisms can be used as a candidate molecular marker to reduce tail fat deposition in sheep.

J-shaped association between the visceral adiposity index and all-cause mortality in patients with chronic kidney disease

ObjectiveVisceral obesity, assessed using the visceral adiposity index (VAI), is related to mortality, but studies of populations with chronic kidney disease (CKD) are scarce. The aim of this study was to evaluate the relationship between VAI and all-cause mortality among individuals with CKD. MethodsWe retrospectively explored the relationship between VAI and risk for all-cause death by analyzing the data of 4145 patients with CKD who participated in the National Health and Nutrition Examination Survey (NHANES) 2001–2006. Patients were followed until December 31, 2015. ResultsAfter an average follow-up of 134.14 mo, 1034 (24.95%) deaths were recorded. Comparison of VAI quartiles with the reference showed an unstable association of VAI with all-cause mortality after adjusting for a wide range of potential confounders in Cox regression analysis. The correlation between VAI and mortality was J-shaped after applying the penalized spline method. Before the inflection point (VAI = 68.23), higher VAI had a protective effect against mortality (hazard ratio [HR], 0.47; 95% confidence interval [CI], 0.28–0.77). However, the risk for all-cause mortality gradually increased with the VAI (HR, 1.13; 95% CI, 1.05–1.21). ConclusionVisceral obesity may influence the rate of all-cause mortality in a nonlinear manner in populations with CKD. Risk for death was higher with visceral fat deficiency than with excessive visceral fat deposition.

Chicken Protein S Gene Regulates Adipogenesis and Affects Abdominal Fat Deposition.

Simple SummaryLow-fat meat is increasingly desired by the public due to the growing popularity of healthy diets, and the excessive accumulation of abdominal fat increases costs in the broiler breeding industry, all of which have encouraged breeding changes in the broiler industry. Investigating fat accumulation at a cellular level from a genetic perspective will help us understand gene-mediated abdominal fat accumulation in chickens. This study aimed to explore the role of the PROS1 gene in adipose cells and its application prospect in broiler breeding. Based on our findings, we found that the PROS1 gene can contribute to adipose cell proliferation and can reduce fat deposits at the cellular level, and its mutations are highly correlated with chicken fat traits.(1) Background: Excessive abdominal fat deposition in broilers not only causes feed waste but also leads to a series of metabolic diseases. It has gradually become a new breeding goal of the broiler industry to improve growth rates and to reduce abdominal fat rates. In a previous study, PROS1 was highly expressed in low-abdominal fat broilers, suggesting a potential role in broilers adipogenesis. However, the function of PROS1 in preadipocytes and its association with abdominal fat traits need to be characterized. (2) Methods: qRT-PCR and Western Blot were used to quantify gene expression at the RNA and protein levels; flow cytometry and EdU were carried out to detect cell proliferation; and a GLM analysis was used to determine the association between PROS1 SNPs and carcass traits. (3) Results: PROS1 was downregulated in high-abdominal fat chicken; PROS1 contributed preadipocyte proliferation but suppressed preadipocyte differentiation; and the SNPs in the PROS1 5′ flank were significantly associated with the abdominal fat weight rate. (4) Conclusions: Chicken PROS1 is able to suppress adipogenesis, and its polymorphisms are associated with the abdominal fat weight rate, which can be considered the molecular markers for chicken breeding, indicating that PROS1 is an effective potential gene in regulating abdominal fat deposition.

Isolation of Preadipocytes from Broiler Chick Embryos

Primary preadipocytes are a valuable experimental system for understanding the molecular pathways that control adipocyte differentiation and metabolism. Chicken embryos provide the opportunity to isolate preadipocytes from the earliest stage of adipose development. This primary cell can be used to identify factors influencing preadipocyte proliferation and adipogenic differentiation, making them a valuable model for studies related to childhood obesity and control of excess fat deposition in poultry. The rapid growth of postnatal adipose tissue effectively wastes feed by allocating it away from muscle growth in broiler chickens. Therefore, methods to understand the earliest stages of adipose tissue development may provide clues to regulate this tendency and identify ways to limit adipose expansion early in life. The present study was designed to develop an efficient method for isolation, primary culture, and adipogenic differentiation of preadipocytes isolated from developing adipose tissue of commercial broiler (meat-type) chick embryos. The procedure has been optimized to yield cells with high viability (~98%) and increased capacity to differentiate into mature adipocytes. This simple method of embryonic preadipocyte isolation, culture, and differentiation supports functional analyses of fat growth and development in early life.

Female Obesity: A Probable Cause of Infertility

Obesity, a serious health problem, is a widespread affliction among women of reproductive age. Obesity and overweight refer to an abnormal and excessive fat deposition that has a negative impact on the body's health. Obesity causes a slew of issues, including social, psychological, demographic, and health issues. It has been associated to elevated health risks like diabetes, hypertension, coronary heart disease, and osteoarthritis, as well as numerous cancers like endometrial, breast, and colon cancers. Hyperandrogenemia is caused by insulin resistance and hyperinsulinemia in obese women. The levels of sex hormone-binding globulin (SHBG) are lower, but leptin levels are higher. Impaired ovulatory function and, as a result, reproductive health could be explained by these changes. Obese women have a reduced probability of giving birth to a healthy infant due to lower implantation and pregnancy rates, greater miscarriage rates, and increased maternal and fetal problems throughout pregnancy. In these people, losing weight has a positive impact on their reproductive outcomes.&#x0D; Keywords: Obesity, Hyperandrogenemia, Sex hormone-binding globulin (SHBG).

Small-quantity lipid-based nutrient supplements, with or without added zinc, do not cause excessive fat deposition in Burkinabe children: results from a cluster-randomized community trial

PurposePublic health interventions to address stunting and wasting should be evaluated for possibly contributing to obesity risk. The present study tested the hypothesis that small-quantity lipid-based nutrient supplements (SQ-LNS) might increase fat deposition, and that additional zinc provided via SQ-LNS or in the form of dispersible tablets would increase fat-free mass (FFM) accretion.MethodsUsing a two-stage, cluster-randomized trial design, 34 communities were randomly assigned to the intervention cohort (IC) or non-intervention cohort (NIC), and family compounds within the IC were randomly assigned to receive different amounts of zinc (0, 5 or 10 mg zinc) incorporated in SQ-LNS or 5 mg zinc in the form of dispersible tablets along with treatment for diarrhea, malaria and fever. Body composition was assessed in a subset of IC (n = 201) and NIC (n = 74) children at 9 and 18 months using the deuterium dilution method. A mixed linear model was used to examine average change in FFM and % fat mass (%FM) among intervention groups and by cohort.ResultsChildren in the IC had significantly greater change in FFM (Mean (95% Confidence Interval)) (1.57 (1.49, 1.64) kg) compared to the NIC (1.35 (1.23, 1.46) kg; p = 0.005). There were no significant differences in the change in %FM between the NIC and IC or among the intervention groups.ConclusionSQ-LNS, along with morbidity treatment increased weight gain and FFM in young children from 9 to 18 months of age without increasing FM deposition. Additional zinc supplementation did not affect changes in FFM or %FM.Trial registrationThe study was registered as a clinical trial with the US National Institute of Health (www.ClinicalTrials.gov; NCT00944281).

Integrative analysis of miRNA and mRNA profiles reveals that gga-miR-106-5p inhibits adipogenesis by targeting the KLF15 gene in chickens

BackgroundExcessive abdominal fat deposition in commercial broilers presents an obstacle to profitable meat quality, feed utilization, and reproduction. Abdominal fat deposition depends on the proliferation of preadipocytes and their maturation into adipocytes, which involves a cascade of regulatory molecules. Accumulating evidence has shown that microRNAs (miRNAs) serve as post-transcriptional regulators of adipogenic differentiation in mammals. However, the miRNA-mediated molecular mechanisms underlying abdominal fat deposition in chickens are still poorly understood. This study aimed to investigate the biological functions and regulatory mechanism of miRNAs in chicken abdominal adipogenesis.ResultsWe established a chicken model of abdominal adipocyte differentiation and analyzed miRNA and mRNA expression in abdominal adipocytes at different stages of differentiation (0, 12, 48, 72, and 120 h). A total of 217 differentially expressed miRNAs (DE-miRNAs) and 3520 differentially expressed genes were identified. Target prediction of DE-miRNAs and functional enrichment analysis revealed that the differentially expressed targets were significantly enriched in lipid metabolism-related signaling pathways, including the PPAR signaling and MAPK signaling pathways. A candidate miRNA, gga-miR-106-5p, exhibited decreased expression during the proliferation and differentiation of abdominal preadipocytes and was downregulated in the abdominal adipose tissues of fat chickens compared to that of lean chickens. gga-miR-106-5p was found to inhibit the proliferation and adipogenic differentiation of chicken abdominal preadipocytes. A dual-luciferase reporter assay suggested that the KLF15 gene, which encodes a transcriptional factor, is a direct target of gga-miR-106-5p. gga-miR-106-5p suppressed the post-transcriptional activity of KLF15, which is an activator of abdominal preadipocyte proliferation and differentiation, as determined with gain- and loss-of-function experiments.Conclusionsgga-miR-106-5p functions as an inhibitor of abdominal adipogenesis by targeting the KLF15 gene in chickens. These findings not only improve our understanding of the specific functions of miRNAs in avian adipogenesis but also provide potential targets for the genetic improvement of excessive abdominal fat deposition in poultry.

MiR-203 is an anti-obese microRNA by targeting apical sodium-dependent bile acid transporter

SummaryObesity is characterized by excessive fat deposition within the body. Bile acids (BA) are important regulators for controlling the absorption of lipid. Here we show that miR-203 exerts weight-loss and lipid-lowering effects by increasing total BA excretion in obese rodents. miR-203 overexpression transgenic mice are resistant to high-fat diet (HFD)-induced obesity and dyslipidemia. Moreover, the knockdown of miR-203 deteriorates metabolic disorders. ASBT plays important role in regulating BA homeostasis and is a direct target of miR-203. In human intestinal epithelial cells, overexpression of miR-203 decreases the cellular uptake of BA by inhibiting ASBT. Furthermore, TCF7L2 is downregulated in obese mice and acts as a transcription factor of miR-203. The ASBT mRNA level was positively correlated with the body mass index (BMI) of population, while the miR-203 level was negatively associated with BMI. Taken together, these data suggest miR-203 could be a new therapeutic BA regulator for obesity and dyslipidemia.

Adipose Tissue Inflammation and Pulmonary Dysfunction in Obesity.

Obesity is a chronic disease caused by an excess of adipose tissue that may impair health by altering the functionality of various organs, including the lungs. Excessive deposition of fat in the abdominal area can lead to abnormal positioning of the diaphragm and consequent reduction in lung volume, leading to a heightened demand for ventilation and increased exposure to respiratory diseases, such as chronic obstructive pulmonary disease, asthma, and obstructive sleep apnoea. In addition to mechanical ventilatory constraints, excess fat and ectopic deposition in visceral depots can lead to adipose tissue dysfunction, which promotes metabolic disorders. An altered adipokine-secretion profile from dysfunctional adipose tissue in morbid obesity fosters systemic, low-grade inflammation, impairing pulmonary immune response and promoting airway hyperresponsiveness. A potential target of these adipokines could be the NLRP3 inflammasome, a critical component of the innate immune system, the harmful pro-inflammatory effect of which affects both adipose and lung tissue in obesity. In this review, we will investigate the crosstalk between adipose tissue and the lung in obesity, highlighting the main inflammatory mediators and novel therapeutic targets in preventing pulmonary dysfunction.

Azadirachta indica Hexane Extract: Potent Antibacterial Activity Against Propionibacterium acne and Identification of its Chemicals Content

Background: Acne is a skin surface disease that appears when the excessive fat deposits clogged the skin pores, causes the growth of acne-causing bacteria and stimulates inflammation. Propionibacterium acnes is one of common acne-causing bacteria which usually manage by synthetic chemical-based drug. However, the presence of its long- used side effects pointed the urgent need of new anti P. acne drug discovery. Azadirachta indica is a medicinal plant which empirically used as antibacterial. A. indica leaves has been reported to exhibit activity against P. acne but limited to ethanol extract. Thus, the evaluation of other extract- and identification of active compound(s) against P. acne is needed to be explore. Methods: First, the microscopic morphology of A. indica leaves were observed using Scanning Electron Microscope. The leaves were then extracted sequentially by hexane, ethyl acetate, and methanol solvent using the ultrasonic assisted extraction method, followed by its in vitro anti- P. acne activity evaluation. The most active extract was further evaluated for its chemical(s) content by LC-MS. Results: Scanning Electron Microscope identified the presence of oxalate in the leaves of A. indica. Evaluation of the anti-P. acne activity showed that the hexane extract had highest anti-P. acne compared to others. Further chemical identification showed that hexane extract contains three steroids, one saturated acids and one phenolic compounds. Conclusions: A. indica hexane extract leaf is prospective to be developed as an acne antibacterial.

Oxidative Stress Can Be Attenuated by 4-PBA Caused by High-Fat or Ammonia Nitrogen in Cultured Spotted Seabass: The Mechanism Is Related to Endoplasmic Reticulum Stress.

Oxidative stress is a common phenomenon in aquaculture, which can be induced by nutritional or environmental factors. Generally, oxidative stress causes poor growth performance, metabolic dysregulation, and even the death of aquatic animals. To identify a nutritional intervention strategy, high-fat diet (HFD) feeding (Experiment I) and acute ammonia nitrogen challenge (Experiment II) tests were carried out. In Experiment I, HFD feeding significantly decreased the growth performance concomitantly with excessive fat deposition in the liver and abdomen. The addition of 4-PBA in the diet improved the excessive fat accumulation. The activities of antioxidative enzymes were suppressed, and the levels of lipid and protein peroxidation were increased, indicating that HFD feeding induced oxidative stress. The endoplasmic reticulum stress (ERs) related genes were downregulated in the HFD group. Under a transmission electron microscope (TEM), more swollen and dilated ER lumen could be observed. These results indicated that the HFD induced ERs activation. Although 4-PBA acted as a potent ERs inhibitor, as evidenced by the alleviated alterations of ERs molecules and the ER ultrastructure, the oxidative stress was also attenuated by 4-PBA. In Experiment II, dietary 4-PBA improved the tolerance to the acute ammonia nitrogen challenge, as lower mortality and serum aminotransferase activity was found. Further results showed that 4-PBA decreased the peroxidation content and attenuated ERs, thus confirming the correlation between oxidative stress and ERs. Our findings showed that dietary 4-PBA supplementation can attenuate oxidative stress induced by a HFD or acute ammonia challenge; the mechanism is related to its potent inhibition effect for ERs.

Betaine Alleviates High-Fat Diet-Induced Disruptionof Hepatic Lipid and Iron Homeostasis in Mice.

Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive fat deposition in the liver, which is often associated with disrupted iron homeostasis. Betaine has been reported to be hepatoprotective, yet whether and how betaine ameliorates high-fat diet-induced disruption of hepatic lipid and iron homeostasis remains elusive. In this study, mice were fed either standard (CON) or high-fat diet (HFD) for 9 weeks to establish a NAFLD model. Mice raised on HF diet were then assigned randomly to HF and HFB groups, HFB group being supplemented with 1% (w/v) of betaine in the drinking water for 13 weeks. Betaine supplementation significantly alleviated excessive hepatic lipid deposition and restored hepatic iron content. Betaine partly yet significantly reversed HFD-induced dysregulation of lipogenic genes such as PRARγ and CD36, as well as the iron-metabolic genes including FPN and HAMP that encodes hepcidin. Similar mitigation effects of betaine were observed for BMP2 and BMP6, the up-stream regulators of hepcidin expression. Betaine significantly rectified disrupted expression of methyl transfer gene, including BHMT, GNMT and DNMT1. Moreover, HFD-modified CpG methylation on the promoter of PRARγ and HAMP genes was significantly reversed by betaine supplementation. These results indicate that betaine alleviates HFD-induced disruption of hepatic lipid and iron metabolism, which is associated with modification of CpG methylation on promoter of lipogenic and iron-metabolic genes.