Excessive Accumulation Of Adipose Tissue Research Articles

1932-P: A Novel Antiobesity Peptide Secreted from Brown Adipocytes

Obesity, the most common metabolic disorder worldwide, is characterized by excess adipose tissue accumulation and causes to serious complications. Many studies have suggested that brown adipocytes contribute to weight loss with increased energy expenditure. Since white adipocytes could be convertible to a “brown-like” state, and induction of browning of white fat also become a promising strategy in the treatment of obesity. Notably, brown fat is not only a heat-producing but also a secretory organ communicating with other metabolic organs. In this study, we focused on peptides secreted by brown adipose tissue to discover new treatment against obesity and metabolic disorder. We successfully obtained a novel polypeptide from the secretory components of brown adipocytes named as BATSP1 (Brown Adipose Tissue Secreted Peptide), which played crucial role in stimulating browning of white adipocytes. The function and mechanism of BATSP1 were comprehensively evaluated in animal models, and we found that administration of BATSP1 stimulated browning of white adipose tissue and elevated mitochondria number dramatically consisting with the activation of energy metabolism. Moreover, to evaluate the feasibility of BATSP1 as a treatment for obesity, we treated DIO mice with BATSP1 and caused significant weight loss as well as decreased glucose and triglyceride content via browning. Taken together, we described an anti-obesity peptide secreted from brown adipocytes, and the underlying mechanism require further study to develop its clinic application. Disclosure Z. Zhang: None. X. Zhang: None. H. Zhong: None. X. Chi: None. X. Cui: None. C. Ji: None. Funding National Natural Science Foundation of China (81770866, 81770837, 81900783)

Insulin resistance in obesity: pathogenesis and effects

The prevalence of obesity in the world is described as the global epidepic. Being not only a chronic recurrent disease but also a serious risk factor, obesity leads to the development and aggravation of many non-communicable diseases. Excessive amount and adipose tissue dysfunction in obesity determines the risk of the development of type 2 diabetes, arterial hypertension, atherosclerosis, non-alcoholic fatty liver disease etc. Secondary insulin resistance often underlies the development of the above mentioned conditions. The mechanisms contributing to the development of insulin resistance in case of excessive adipose tissue accumulation are being intensively investigated over the last decades, however many questions yet remain unsolved. In this article we present the key mechanisms underlying insulin resistance in obesity and diagnostic approaches for insulin resistance as well as the current data in this topic. The authors review the close links between insulin resistance and obesity related diseases, namely disorders of carbohydrate metabolism, dyslipidemia, arterial hypertension, coronary artery disease and reproductive disorders.

Obesity and Circadian Cycle of Sleep and Wakefulness: Common Points and Prospects of Therapy

The prevalence of obesity in recent years has assumed the character of a non-communicable epidemic. Wherein, the standard approaches for its treatment are not always successful. Meanwhile, obesity remains one of the main causes of the formation of a number of some serious diseases, such as cardiovascular, diabetes, cancer, etc. and death from them. In search of alternative and more adequate methods of obesity treatment and preventing its complications, recent studies are aimed at further identifying new associations and revealing the pathophysiological mechanisms underlying excessive weight gain. It should be noted an increasing amount of chronobiological studies that raised awareness of the key role of the body’s circadian rhythms and its main regulator, melatonin, responsible for the temporary organization of the main physiological (including metabolism) processes throughout the 24-h day, in the development and progression of obesity. This review is devoted to the consideration of mutually directed interactions between the circadian system and metabolism; attempts have been made to explain the role of sleep-wake cycle disruptions in the excess accumulation of adipose tissue and the formation of obesity and its comorbidities, as well as detailed therapeutic principles based on normalizing disruption of body clocks using time-coordinated approaches to food intake, physical activity, the effects of non-drug methods and pharmacological substances (chronobiotics), which represents a novel and promising ways to prevent or treat obesity and associated diseases.

Pilot study and bioinformatics analysis of differentially expressed genes in adipose tissues of rats with excess dietary intake.

Excessive adipose tissue accumulation is an increasing health problem worldwide. The present study aimed to determine differentially expressed genes (DEGs) that are associated with the excessive accumulation of adipose tissues by PCR arrays in an excess dietary intake animal model. For this purpose, male Sprague Dawley rats were randomly assigned to 2 groups: Control (given an ordinary diet) and experimental (given twice the amount of the ordinary diet). After 2 months of feeding, the abdominal cavities of the rats from each group were opened, then subcutaneous and visceral adipose tissues were removed. The adipose tissues collected were then used for total RNA extraction and then reverse transcribed to cDNA, which was then used as a template to identify the DEGs of 84 transcripts for rat obesity by RT2 Profiler PCR Arrays. The results showed significant downregulation of bombesin-like receptor 3 (BRS3) and uncoupling protein 1 (UCP1) in visceral adipose tissues of experimental rats compared with those of the control rats, and differential gene expression analysis showed an association with fat cell differentiation and regulation of triglyceride sequestration, as well as fatty acid binding. The gene expression patterns observed in the present study, which may be associated with peroxisome proliferator-activated receptor-γ (PPARG) on excessive visceral adipose tissue accumulation, may be useful in identifying a group of surrogate biomarkers for the early diet-induced accumulation of visceral adipose tissue detection in humans. The biomarkers can also be the specific targets for drug development to reduce excessive visceral adipose tissue accumulation in the body and its associated diseases.

Obesity, adipose tissue, and bariatric surgery.

Obesity prevalence has increased in the last decades worldwide leading to metabolic complications, such as type 2 diabetes, steatosis, cardiovascular disease, among others; its development is influenced by genetic factors and environmental factors, such as intestinal microbiome. In Mexico, 33.3% of the adults present this disease. Obesity is defined as an excessive adipose tissue accumulation, provoking its dysfunction. Adipose tissue remodeling, which involves angiogenesis, hypoxia and inflammation, is implicated in the developing of obesity and metabolic modifications. Bariatric surgery is the most used and successful intervention to control morbid obesity, leading a maintained loss of weight and remission of some of its comorbidities as type 2 diabetes. Here, we review some of the molecular aspects of the metabolic changes provoked by bariatric surgery and its impact in weight loss and comorbidities remission. In summary, this article reviews the genetic aspects, microbiome and molecular facts (adipose tissue remodeling) that are involved in obesity development. In addition, some of the molecular aspects about bariatric surgery are described and the mechanisms that are regulated to control obesity and its comorbidities.

Increased visceral adipose tissue in male patients with non-clear cell renal cell carcinoma.

It is well known that there is a link between obesity and oncogenesis in many sites, including the kidney. Adiposopathy is characterized by an excessive accumulation of adipose tissue, principally visceral, which can lead to adipocyte and adipose tissue-related disorder, promoting metabolic syndrome. Visceral adipocytes secrete growth factors, proinflammatory cytokines and adipokines, regarded as mediating factors associated with the oncogenesis of obesity-related tumors. In this study, we evaluate the relationship between visceral adipose tissue (VAT) and non-clear cell renal cell carcinoma (nccRCC) in male patients. In this retrospective study, two groups were included: nccRCC group and control group. Total adipose tissue (TAT) area, VAT area and subcutaneous adipose tissue (SAT) area were measured in both groups. VAT/SAT ratio was subsequently calculated. Statistically significant differences between the two groups were found in TAT area (p = 0.05), VAT area (p < 0.01) and VAT/SAT ratio (p < 0.05), while no significant difference was found in SAT area. This study demonstrates an increased visceral adipose tissue in male patients with nccRCC.

Genetic deletion of mast cell serotonin synthesis prevents the development of obesity and insulin resistance

Obesity is linked with insulin resistance and is characterized by excessive accumulation of adipose tissue due to chronic energy imbalance. Increasing thermogenic brown and beige adipose tissue futile cycling may be an important strategy to increase energy expenditure in obesity, however, brown adipose tissue metabolic activity is lower with obesity. Herein, we report that the exposure of mice to thermoneutrality promotes the infiltration of white adipose tissue with mast cells that are highly enriched with tryptophan hydroxylase 1 (Tph1), the rate limiting enzyme regulating peripheral serotonin synthesis. Engraftment of mast cell-deficient mice with Tph1−/− mast cells or selective mast cell deletion of Tph1 enhances uncoupling protein 1 (Ucp1) expression in white adipose tissue and protects mice from developing obesity and insulin resistance. These data suggest that therapies aimed at inhibiting mast cell Tph1 may represent a therapeutic approach for the treatment of obesity and type 2 diabetes.

Inter-relationship among abdominal obesity cardiorespiratory fitness, and body image attitude among menopausal women in Oyo state Nigeria

Introduction Abdominal obesity is the accumulation of excess adipose tissue in the abdomen. Hormonal changes in menopausal women may lead to physical inactivity which results in decreased cardiorespiratory fitness and increase in incidence of obesity. Cardiorespiratory fitness is one of the strongest predictors of cardiovascular health and longevity and a useful health indicator. The interrelationship among abdominal obesity, cardiorespiratory fitness and body image attitude among menopausal women was investigated in this study. Method A cross-sectional survey method was adopted, using purposive sampling to recruit women from Iseyin Local Government Area, Oyo State, Nigeria. Premenopausal, perimenopausal and postmenopausal women had their abdominal obesity, cardiorespiratory fitness and body image attitude assessed using waist circumference, six minute-walk test and multidimensional body-self relations questionnaire (MBSRQ) respectively. Data were analysed using descriptive and inferential statistics with ᾳ = 0.05. Results Participants comprised 381 women aged 47.1±8.6 years, they had low mean estimated maximum oxygen consumption of 10.81±1.77ml/kg/min. The postmenopausal women had the highest median score of abdominal obesity of 96.0 (20.0) cm. A positive and significant weak correlation of abdominal obesity with cardiorespiratory fitness was observed among the premenopausal (r=0.156; p=0.050) women while negative and non-significant correlations were observed in both the perimenopausal and postmenopausal groups. Cardiorespiratory fitness and abdominal obesity exhibited varied correlations with body image attitude variables of menopausal women. Conclusion Cardiorespiratory fitness and abdominal obesity were somewhat indirectly correlated in the older menopausal women. They also exhibited variable correlations toward body image.

MiRNAs and Novel Food Compounds Related to the Browning Process.

Obesity prevalence is rapidly increasing worldwide. With the discovery of brown adipose tissue (BAT) in adult humans, BAT activation has emerged as a potential strategy for increasing energy expenditure. Recently, the presence of a third type of fat, referred to as beige or brite (brown in white), has been recognized to be present in certain kinds of white adipose tissue (WAT) depots. It has been suggested that WAT can undergo the process of browning in response to stimuli that induce and enhance the expression of thermogenesis: a metabolic feature typically associated with BAT. MicroRNAs (miRNAs) are small transcriptional regulators that control gene expression in a variety of tissues, including WAT and BAT. Likewise, it was shown that several food compounds could influence miRNAs associated with browning, thus, potentially contributing to the management of excessive adipose tissue accumulation (obesity) through specific nutritional and dietetic approaches. Therefore, this has created significant excitement towards the development of a promising dietary strategy to promote browning/beiging in WAT to potentially contribute to combat the growing epidemic of obesity. For this reason, we summarize the current knowledge about miRNAs and food compounds that could be applied in promoting adipose browning, as well as the cellular mechanisms involved.

Otyłość w chorobach przewlekłych u dzieci

Obesity develops as a result of long-term positive energy balance, with the participation of genetic, environmental factors and comorbidities. Obesity and overweight is currently one of the major health problems in many countries around the world, including Poland. The problem of excessive body mass is also increasingly affecting children and adolescents, and the number of overweight or obese people is rising fast in this group. Currently, every fifth child in Poland is obese or overweight. As overweight, we define excessive accumulation of adipose tissue, that does not meet the criteria for diagnosing obesity (BMI 85-95th percentile). Obesity is defined as excessive accumulation of adipose tissue leading to eterioration of health (&gt; 95th percentile). Overweight and obesity coexist with many chronic diseases and complicates the course of comorbidities. Excessive body weight is an important risk factor of premature death. Obesity prevention and treatment can improve the course of co-morbid diseases and should be the basis of patient care.

Quercetin and Epigallocatechin Gallate in the Prevention and Treatment of Obesity: From Molecular to Clinical Studies.

Obesity is a worldwide epidemic, which is characterized by the excess accumulation of adipose tissue and to an extent that impairs both the physical and psychosocial health and well-being. There are several weight-loss strategies available, including dietary modification, pharmacotherapy, and bariatric surgery, but many are ineffective or not a long-term solution. Bioactive compounds present in medicinal plants and plant extracts, like polyphenols, constitute the oldest and most extensive form of alternative treatments for the prevention and management of obesity. Their consumption is currently increasing in the population due to the high cost, potential adverse effects, and limited benefits of the currently available pharmaceutical drugs. A great number of studies has explored how dietary polyphenols can interfere with the different mechanisms associated with obesity development. They suggest that these compounds can decrease energy and food intake, lipogenesis, and preadipocyte differentiation and proliferation, while increasing energy expenditure, lipolysis, and fat oxidation. Both quercetin, one of the most common dietary flavonols in the western diet, and epigallocatechin gallate (EGCG), the most abundant polyphenol in green tea, exhibit antiobesity effects in adipocyte cultures and animal models. However, the extrapolation of these potential benefits to obese humans remains unclear. Although quercetin supplementation does not seem to exert any beneficial effects on body weight, this polyphenol could prevent the obesity-associated mortality by reducing cardiovascular disease risk. An important consideration for the design of further trials is the occurrence of gene polymorphisms in key enzymes involved in flavanol metabolism, which determines a subject's sensitivity to catechins and seems, therefore, crucial for the success of the antiobesity intervention. Although the evidence supporting antiobesity effects is more consistent in EGCG than with quercetin studies, they could still be beneficial by reducing the cardiovascular risk of obese subjects, rather than inducing body weight loss.

Mechanisms Involved in Childhood Obesity-Related Bone Fragility.

Childhood obesity is one of the major health problems in western countries. The excessive accumulation of adipose tissue causes inflammation, oxidative stress, apoptosis, and mitochondrial dysfunctions. Thus, obesity leads to the development of severe co-morbidities including type 2 diabetes mellitus, liver steatosis, cardiovascular, and neurodegenerative diseases which can develop early in life. Furthermore, obese children have low bone mineral density and a greater risk of osteoporosis and fractures. The knowledge about the interplay bone tissue and between adipose is still growing, although recent findings suggest that adipose tissue activity on bone can be fat-depot specific. Obesity is associated to a low-grade inflammation that alters the expression of adiponectin, leptin, IL-6, Monocyte Chemotactic Protein 1 (MCP1), TRAIL, LIGHT/TNFSF14, OPG, and TNFα. These molecules can affect bone metabolism, thus resulting in osteoporosis. The purpose of this review was to deepen the cellular mechanisms by which obesity may facilitate osteoporosis and bone fractures.

Thermoregulatory Changes in Obese Mexican Young Women Performing Aerobic Exercise

Mexico has the highest rate of obesity worldwide. This pandemic is defined as an abnormal and excessive accumulation of adipose tissue providing an insulating layer that impedes heat loss, thus affecting body homeostasis. To maintain normothermia, obese individuals must increase heat dissipation. Here, we explore the potential role of thermoregulation in obese young Mexican women performing aerobic exercise in order to determine how thermoregulation mechanisms act in such conditions. A group of 60 obese (O), overweight (OW) and normal (N) women, with 20 in each group, performed a 15 min test on the cycle‐ergometer at a 65% heart rate (HR) at room temperature (21.0±0.5) °C and under extreme temperature (38.5±0.5) °C conditions. Body mass index (BMI) and % body fat were calculated. HR, blood pressure (Bp), and core (Tc) and external (Te) temperatures were measured during and after the test. We observed a difference in Tc within subjects and within groups. At room and extreme temperatures, OW and O subjects presented higher Tc compared to N ones by about 30%, adding that the initial Tc of O was higher (15%) compared to the other two groups. N women tended to reach their initial temperature faster than the other groups at room and extreme temperatures. A 45% increment of HR was observed in O compared to OW and N women. From our results we concluded that there exists a direct relation between BMI and the thermoregulatory capacity in the human body, suggesting a failure in homeostasis processes in obese women. This experiment gives us the first insight of an active indicator of a metabolic decompensation in young Mexican women and compelling evidence for a thermogenic handicap in the same population. Further analyses have to be done.Support or Funding InformationSupported partially by UNAM (PAPIIT RA207818) to KPGPThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Gut microbiota: a new path to treat obesity.

Obesity is a multifactorial disease resulting in excessive accumulation of adipose tissue. Over the last decade, growing evidence has identified the gut microbiota as a potential factor in the pathophysiology of both obesity and the related metabolic disorders. The gut microbiota is known to protect gastrointestinal mucosa permeability and to regulate the fermentation and absorption of dietary polysaccharides, perhaps explaining its importance in the regulation of fat accumulation and the resultant obesity. The proposed mechanisms by which the gut microbiota could contribute to the pathogenesis of obesity and the related metabolic diseases include: (a) a high abundance of bacteria that ferment carbohydrates, leading to increased rates of short-chain fatty acid (SCFA) biosynthesis, providing an extra source of energy for the host, that is eventually stored as lipids or glucose; (b) increased intestinal permeability to bacterial lipopolysaccharides (LPS), resulting in elevated systemic LPS levels that aggravate low-grade inflammation and insulin resistance; (c) increased activity of the gut endocannabinoid system. Fecal transplantation studies in germ-free mice have provided crucial insights into the potential causative role of the gut microbiota in the development of obesity and obesity-related disorders. Diet +/- bariatric surgery have been reported to modulate the gut microbiota, leading to lean host phenotype body composition. This review aims to report clinical evidence for a link of the gut microbiota with human obesity and obesity-related diseases, to provide molecular insights into these associations, and to address the effect of diet and bariatric surgery on the gut microbiota, including colonic microbiota, as a potential mechanism for promoting weight loss.

Muscle Fitness Changes During Childhood Associates With Improvements in Cardiometabolic Risk Factors: A Prospective Study.

The role of muscle fitness in controlling cardiometabolic risk factors during childhood is incompletely understood. A prospective observational design including 6- to 11-year-old children (n = 512) was used to study associations between 1.5-year changes in handgrip strength, standing vertical jump displacement, the short shuttle run, and a composite of these with changes in composite and single cardiometabolic risk markers. The authors modeled sequential mixed linear regressions controlling for changes in cardiorespiratory fitness, waist circumference, and other putative confounding variables. Statistically significant associations, standardized beta (95% confidence intervals), were observed between changes in composite muscle fitness -0.19 (-0.30 to -0.07), muscular strength -0.15 (-0.25 to -0.06), and agility 0.14 (0.04 to 0.23), but not muscular power -0.06 (-0.14 to 0.03) with changes in the composite risk score. In sex-stratified analysis, associations were robust in girls, but not in boys. Control for changes in cardiorespiratory fitness and waist circumference greatly attenuated associations. Changes in muscle fitness were strongly associated with changes in waist circumference in both girls -0.21 (-0.37 to -0.05) and boys -0.23 (-0.35 to -0.11) after controlling for cardiorespiratory fitness. Our data support a unique role of muscle fitness in the promotion of metabolic health and prevention of excess adipose tissue accumulation in children.

Web of Causation between Dietary Patterns and Childhood Obesity: Applying Hill's Criteria

Abstract Since their publication in 1965, the Bradford Hill criteria for causality have been largely used as a framework for causal inference in epidemiology. We aim at employing this classical approach to shed new light onto the web of causation of childhood obesity. Although the fundamental cause of obesity is the long-term imbalance between energetic need and intake, this medical condition is multifactorial in its origin, influenced by genetic, behavioral, socioeconomic, and environmental factors. This imbalance leads to accumulation of excessive adipose tissue. Observational studies tend to mostly quantify association between dietary factors and accumulation of adipose tissue. On the other hand, multivariate analysis proved some of these associations to be spurious, therefore prospective trials are needed to demonstrate causality. Short term experimental studies have been conducted to identify unique dietary pattern changes on specific outcomes, but long term, community-based studies would offer more comprehensive answers on dietary pattern effects. We conducted a literature review on PubMed, Scopus, Web of Science, and Google Scholar. From a total of 323 papers identified at first stage, we further discuss the applicability of Bradford Hill criteria for 31 articles, by examples of dietary patterns and accumulation of excess body fat as exposure-response associations. We also put forward and analyzed the evidence prospective studies would bring, as foundation for future interventions.

Neuropeptide receptors as potential pharmacological targets for obesity.

Obesity is a chronic multifactorial disease, characterized by an excessive accumulation of adipose tissue. It is usually the result of excessive food intake and/or low energy expenditure. Obesity can be triggered by lifestyle, nutritional, genetic, environmental, hormonal and psychological factors. Several strategies are used to treat obesity, including dietary reeducation, with balanced food intake, increased physical exercise, in order to promote energy expenditure and to overcome the insufficiency in weight reduction by other strategies, and administration of drugs. However, these medications are associated to undesirable side effects, resulting in a high withdrawal rate. Several studies have been focused on the development of compounds that act in the hypothalamic region where the center of the regulation of hunger and satiety is located. Some of them target the activity of endogenous peptides, such as ghrelin pancreatic polypeptide, peptide YY and neuropeptide Y, as well as their receptors. This review addresses the importance of understanding the neuropeptide/peptide hormones and their receptors for the development of novel anti-obesity compounds that may aid in weight reduction as a promising alternative for the treatment of obesity.

Assessment of the Effect of Dietary Modifications and Bioenteric Intragastric Balloon Treatment on the Changes of Some Morphological and Biochemical Parameters in Obese Patients

Obesity is the most common disease of affluence of the XXI century. According to WHO (World Health Organization), it is defined as a chronic metabolic disorder manifested by excessive accumulation of adipose tissue with high tendency for familial occurrence. According to WHO, obesity reaches epidemic proportions in many countries. High BMI (Body Mass Index) correlates with coexisting diseases. Traditional dietetic treatment often does not bring any results. A form of conservative (non-surgical) support for patients in fighting with obesity is the reduction of stomach volume by bioenteric intragastric balloon (BIB) treatment. The aim of the work was to develop a diet with anti-inflammatory properties, well-tolerated by the patients after BIB treatment. An American diet was modified by changing the composition of fatty acids, increasing anti-oxidative potential and adding synbiotics for patients treated with BIB. Chemical analysis of reconstructed food ratios of recommended diet was performed, analysing the content of micronutrients, composition of fatty acids, antioxidative capacity, reducing power and the content of polyphenols. Improvement in anthropometric measurement results and satisfying body weight loss were obtained, while preserving fat-free body mass. Improvement in the parameters of lipid metabolism was also observed, that is, decrease in total CH (cholesterol) and TG (triglycerides), and normalized concentration of HDL (high density lipoproteins) and LDL (low density lipoproteins) fractions. Reduced concentration of glucose in blood and lower blood pressure was also noted. Performed study confirms the effectiveness of complex treatment with BIB and properly adjusted individualized diet. Observations and own experience allow to deduce that patients who resign from systematic contact with a dietician cannot maintain reduced body weight. Abandoning previous habits is the only way to maintain the effect of weight loss. Most importantly, the change in patients’ awareness and consequent behaviour in the future are crucial. Even though genes may contribute to obesity, environmental factors mainly determine the possibility of the disease to occur. Therefore, the change of patients’ lifestyle after body weight reduction will decide on their fate.

PPARγ Controls Ectopic Adipogenesis and Cross-Talks with Myogenesis During Skeletal Muscle Regeneration.

Skeletal muscle is a regenerative tissue which can repair damaged myofibers through the activation of tissue-resident muscle stem cells (MuSCs). Many muscle diseases with impaired regeneration cause excessive adipose tissue accumulation in muscle, alter the myogenic fate of MuSCs, and deregulate the cross-talk between MuSCs and fibro/adipogenic progenitors (FAPs), a bi-potent cell population which supports myogenesis and controls intra-muscular fibrosis and adipocyte formation. In order to better characterize the interaction between adipogenesis and myogenesis, we studied muscle regeneration and MuSC function in whole body Pparg null mice generated by epiblast-specific Cre/lox deletion (PpargΔ/Δ). We demonstrate that deletion of PPARγ completely abolishes ectopic muscle adipogenesis during regeneration and impairs MuSC expansion and myogenesis after injury. Ex vivo assays revealed that perturbed myogenesis in PpargΔ/Δ mice does not primarily result from intrinsic defects of MuSCs or from perturbed myogenic support from FAPs. The immune transition from a pro- to anti-inflammatory MuSC niche during regeneration is perturbed in PpargΔ/Δ mice and suggests that PPARγ signaling in macrophages can interact with ectopic adipogenesis and influence muscle regeneration. Altogether, our study demonstrates that a PPARγ-dependent adipogenic response regulates muscle fat infiltration during regeneration and that PPARγ is required for MuSC function and efficient muscle repair.

An Experimental Model of Hepatic Steatosis to Detect Lipid Accumulation

Obesity is associated with an increased risk of metabolic syndromes such as type 2 diabetes, insulin resistance, dyslipidaemia and non-alcoholic fatty liver disease. Obesity occurs as a result of an imbalance between food intake and energy expenditure leading to excessive accumulation of adipose tissue. NAFLD is the most common liver condition and related to the resistance of insulin. Insulin resistance is associated with an increased influx of lipid into the liver promoting accumulation of hepatic triglyceride. This study aims to develop an experimental model of hepatic steatosis with lipid over-accumulation. HepG2 cells were cultured for 24 hours in free fatty acid media (1:2 palmitic acid and oleic acid respectively). Intracellular lipid content and lipotoxicity were determined by oil red O staining followed by colorimetric detection. This experiment was accomplished by defining the experimental conditions of lipid exposure that leads to significant intracellular fat accumulation in the absence of lipotoxicity with 1 mM of free fatty acid media. As a result, oleic and palmitic acids could be over-accumulated in HepG2 cells. 1 mM free fatty acid media did not affect the cell integrity and did not cause lipotoxicity of the cells.