Variation in Lifestyle-Related Behavior Among Obese Indian Patients With Non-alcoholic Fatty Liver Disease.
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ABSTRACT:
SUBMITTER: Arora C
PROVIDER: S-EPMC8079655 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Recent reports suggest a role for the Patatin-like phospholipase domain-containing protein 3 (PNPLA3) in the pathology of non-alcoholic fatty liver disease (NAFLD). Lipid deposition in the liver seems to be a critical process in the pathogenesis of NAFLD. The aim of the present work was to evaluate the association between the liver PNPLA3 expression, key genes of lipid metabolism, and the presence of NAFLD in morbidly obese women. We used real-time polymerase chain reaction (PCR) analysis to analyze the hepatic expression of PNPLA3 and lipid metabolism-related genes in 55 morbidly obese subjects with normal liver histology (NL, n = 18), simple steatosis (SS, n = 20), and non-alcoholic steatohepatitis (NASH, n = 17). Liver biopsies were collected during bariatric surgery. We observed that liver PNPLA3 expression was increased in NAFLD than in NL. It was also upregulated in SS than in NL. Interestingly, we found that the expression of PNPLA3 was significantly higher in severe than mild SS group. In addition, the expression of the transcription factors LXRα, PPARα, and SREBP2 was positively correlated with PNPLA3 liver expression. Regarding rs738409 polymorphism, GG genotype was positive correlated with the presence of NASH. In conclusion, our results show that PNPLA3 could be related to lipid accumulation in liver, mainly in the development and progression of simple steatosis.
| S-EPMC4881456 | biostudies-literature
Project description:Non-alcoholic fatty liver disease (NAFLD), one of the most common causes of liver disease, is an increasingly common cause of hepatocellular carcinoma (HCC). Several demographic, clinical, and genetic factors contribute to HCC risk in NAFLD patients, which may inform risk stratification scores. Proven efficacious approaches to primary prevention approach in patients with non-viral liver disease remain an area of need. Semi-annual surveillance is associated with improved early tumor detection and reduced HCC-related mortality; however, patients with NAFLD have several challenges to effective surveillance, including under-recognition of at-risk patients, low surveillance utilization in clinical practice, and lower sensitivity of current tools for early-stage HCC detection. Treatment decisions are best made in a multidisciplinary fashion and are informed by several factors including tumor burden, liver dysfunction, performance status, and patient preferences. Although patients with NAFLD often have larger tumor burden and increased comorbidities compared to counterparts, they can achieve similar post-treatment survival with careful patient selection. Therefore, surgical therapies continue to provide a curative treatment option for patients diagnosed at an early stage. Although there has been debate about the efficacy of immune checkpoint inhibitors in patients with NAFLD, current data are insufficient to change treatment selection based on liver disease etiology.
| S-EPMC10202236 | biostudies-literature
Project description:Nonalcoholic fatty liver disease (NAFLD) is well described as a common cause of chronic liver disease, mostly in the obese population. It refers to a spectrum of chronic liver disease that starts with simple steatosis than progresses to nonalcoholic steatohepatitis and cirrhosis in patients without significant alcohol consumption. NAFLD in the non-obese population has been increasingly reported and studied recently. The pathogenesis of nonobese NAFLD is poorly understood and is related to genetic predisposition, most notably patatin-like phospholipase domain-containing 33 G allele polymorphism that leads to intrahepatic triglyceride accumulation and insulin resistance. Non-obese NAFLD is associated with components of metabolic syndrome and, especially, visceral obesity which seems to be an important etiological factor in this group. Dietary factors and, specifically, a high fructose diet seem to play a role. Cardiovascular events remain the main cause of mortality and morbidity in NAFLD, including in the non-obese population. There is not enough data regarding treatment in non-obese NAFLD patients, but similar to NAFLD in obese subjects, lifestyle changes that include dietary modification, physical activity, and weight loss remain the mainstay of treatment.
| S-EPMC5561430 | biostudies-literature
Project description:Background and aimNon-alcoholic fatty liver disease (NAFLD) can progress in non-obese patients as in obese patients. Reports on long-term prognosis in non-obese NAFLD patients are controversial. Therefore, we aimed to examine the long-term prognosis of non-obese patients with NAFLD.MethodsThis single-center, retrospective cohort study enrolled biopsy-proven non-obese and obese NAFLD patients between January 2002 and December 2011 and followed them up until 31 March 2021, for death and clinical events (cardiovascular and liver-related events and extrahepatic cancers).ResultsOf the 223 NAFLD patients, 58 (26.0%) were non-obese. Compared with obese patients, they had a lower fibrosis stage (0.8 ± 0.80 vs 1.2 ± 0.91; P = 0.004), milder lobular inflammation (0.9 ± 0.7 vs 1.1 ± 0.7; P = 0.02), and significantly lower serum creatinine, total bilirubin, ferritin, and type IV collagen 7S and higher high-density lipoprotein levels. After a median follow-up of 8.9 years, no significant difference was noted in mortality between the two groups (2 [3.4%] non-obese vs 5 [3.0%] obese; log-rank test, P = 0.63). Twelve patients (20.7%) in the non-obese group and 32 (19.4%) in the obese group had clinical events. Although the obese group had a higher incidence of clinical events during the first 10 years of follow-up, the non-obese group had a higher incidence after that (log-rank test, P = 0.67). The non-obese group had a high incidence of malignancy (9 [15.5%] non-obese vs 14 [8.3%] obese; P = 0.13).ConclusionNon-obese NAFLD does not necessarily have a good prognosis, and some cases have a poor prognosis such as extrahepatic cancers. Further validation is required in the future.
| S-EPMC9575321 | biostudies-literature
Project description:Fructose intake is associated with non-alcoholic fatty liver disease (NAFLD) development.The objective of this study was to measure fructose absorption/metabolism in paediatric NAFLD compared with obese and lean controls.Children with histologically proven NAFLD, and obese and lean controls received oral fructose (1?g?kg(-1) ideal body weight). Serum glucose, insulin, uric acid, and fructose, urine uric acid, urine fructose, and breath hydrogen levels were measured at baseline and multiple points until 360?min after fructose ingestion.Nine NAFLD (89% Hispanic, mean age 14.3 years, mean body mass index [BMI] 35.3?kg?m(-2)), six obese controls (67% Hispanic, mean age 12.7 years, mean BMI 31.0?kg?m(-2)) and nine lean controls (44% Hispanic, mean age 14.3 years, mean BMI 19.4?kg?m(-2)) were enrolled. Following fructose ingestion, NAFLD vs. lean controls had elevated serum glucose, insulin and uric acid (P?<?0.05), higher urine uric acid (P?=?0.001), but lower fructose excretion (P?=?0.002) and lower breath hydrogen 180-min AUC (P?=?0.04). NAFLD vs. obese controls had similar post-fructose serum glucose, insulin, urine uric acid and breath hydrogen, but elevated serum uric acid (P?<?0.05) and lower urine fructose excretion (P?=?0.02).Children with NAFLD absorb and metabolize fructose more effectively than lean subjects, associated with an exacerbated metabolic profile following fructose ingestion.
| S-EPMC4948988 | biostudies-literature
Project description:Dysregulation of several metabolite pathways, including branched-chain amino acids (BCAAs), are associated with Non-Alcoholic Fatty Liver Disease (NAFLD) and insulin resistance in adults, while studies in youth reported conflicting results. We explored whether, independently of obesity and insulin resistance, obese adolescents with NAFLD display a metabolomic signature consistent with disturbances in amino acid and lipid metabolism. A total of 180 plasma metabolites were measured by a targeted metabolomic approach in 78 obese adolescents with (n = 30) or without (n = 48) NAFLD assessed by magnetic resonance imaging (MRI). All subjects underwent an oral glucose tolerance test and subsets of patients underwent a two-step hyperinsulinemic-euglycemic clamp and/or a second MRI after a 2.2 ± 0.8-year follow-up. Adolescents with NAFLD had higher plasma levels of valine (p = 0.02), isoleucine (p = 0.03), tryptophan (p = 0.02), and lysine (p = 0.02) after adjustment for confounding factors. Circulating BCAAs were negatively correlated with peripheral and hepatic insulin sensitivity. Furthermore, higher baseline valine levels predicted an increase in hepatic fat content (HFF) at follow-up (p = 0.01). These results indicate that a dysregulation of BCAA metabolism characterizes obese adolescents with NAFLD independently of obesity and insulin resistance and predict an increase in hepatic fat content over time.
| S-EPMC5537762 | biostudies-literature
Project description:A significant proportion of patients with non-alcoholic fatty liver disease (NAFLD) in Asian sub-continent are non-overweight and may have different underlying risk factors, lifestyles and metabolic profiles. Seven hundred fifty patients of NAFLD with raised alanine-amino-transferase (ALT) were divided into non-overweight and obese group based on their body mass index (BMI). Detailed dietary and lifestyle history were obtained through questionnaires and a detailed assessment of metabolic profile and liver stiffness was done. Normal BMI (<?23 kg/m2) was found in 6.6% patients, of which 69.5% had raised ALT. Though the intake of dietary fat and exercise pattern were not different amongst these groups, yet the amount of aerated drinks was higher in obese subjects (12?±?17 vs. 7?±?7.5 p?=?0.005). Serum low-density lipoprotein (111?±?25.6 vs. 127.7?±?32.7 p?=?0.04) and insulin resistance based on HOMA-IR?>?2 were significantly higher in obese group (4.1?±?0.36 vs. 2.0?±?0.15 p?=?0.001). Insulin resistance and dyslipidemia were prevalent in 12% and 25% non-overweight patients respectively. Metabolic syndrome was more common in obese subjects. In addition, magnetic resonance elastography showed higher mean liver fat in the obese group with similar hepatic fibrosis. Non-overweight patients with NAFLD had lower insulin resistance and prevalence of dyslipidaemia at similar dietary and exercise pattern.
| S-EPMC7499301 | biostudies-literature
Project description:Non-alcoholic fatty liver disease (NAFLD) is an excessive accumulation of fat in the liver without alcohol abuse. It is linked to metabolic syndrome (MetS) and no pharmacological treatment exists. This systematic review aims to assess evidence about the effect of Mediterranean lifestyle on the prevention and reversion of NAFLD. A systematic literature search was performed in MEDLINE via Pubmed. MeSH terms used were: non-alcoholic fatty liver disease [MeSH Major Topic] AND metabolic syndrome [MeSH Term] AND (Diet, Mediterranean [MeSH Term]) OR (Exercise [MeSH Term]). (PROSPERO ID: 2021 CRD42021289495). Thirteen articles were selected and divided into two categories (four focused on Mediterranean diet and NAFLD and nine focused on Mediterranean diet, physical activity, and NAFLD). Information of clinical endpoints was based on NAFLD, as well as MetS, body mass index, fasting glycemia, obesity, cholesterol, triglycerides, transaminases, albuminuria, and hepatic steatosis, among others. All studies found beneficial associations between the clinical parameters of NAFLD/MetS and following a Mediterranean diet and regular physical activity. An effective treatment that prevents, and even reverses, NAFLD is to adapt lifestyle to the Mediterranean one, based on a Mediterranean diet and regular physical activity.
| S-EPMC8746321 | biostudies-literature
Project description:Nonalcoholic fatty liver disease (NAFLD), ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), and eventually cirrhosis and liver failure, is seen to be increasing amongst Western children. NAFLD rates are rising in parallel with the epidemic of childhood obesity, and in particular, fatty liver evolves more easily in NASH when poor dietary habits and sedentary lifestyle are combined. In fact, its general prevalence in the child population varies between 2.6% and 10%, but increases up to 80% in obese children. Since NASH is expected to become the most common cause of pediatric chronic liver disease in the near future, there is broad interest amongst clinical researchers to move forward, both in diagnosis and treatment. Unfortunately, to date, the expensive and invasive procedure of liver biopsy is seen as the gold standard for NASH diagnosis and few noninvasive diagnostic methods can be applied successfully. Moreover, there are still no approved pharmacological interventions for NAFLD/NASH. Therefore, current management paradigms are based upon the presence of associated risk factors and aims to improve an individual's quality of life, thus reducing NAFLD-associated morbidity and mortality. Today, lifestyle intervention (diet and exercise) is the treatment of choice for NAFLD/NASH. Thus far, no study has evaluated the potential preventive effect of lifestyle intervention on children at risk of NAFLD/NASH. Future studies will be required in this area with the perspective of developing a national program to promote nutrition education and increase physical activity as means of preventing the disease in individuals at risk. Here, we outline the clinical course, pathogenesis and management of NAFLD in children, highlighting the preventive and therapeutic value of lifestyle intervention.
| S-EPMC2797656 | biostudies-literature
Project description:BackgroundGiven the high prevalence of non-alcoholic fatty liver disease (NAFLD) in obese children, non-invasive markers of disease to date are still limited and worth exploring.ObjectiveThis study aimed to evaluate the association between inflammatory markers and NAFLD in obese children.MethodsWe performed a case-control study in Hunan Children's Hospital from September 2020 to September 2021. Study participants were children with obesity diagnosed with NAFLD by abdominal ultrasound examination. Mean platelet volume (MPV), platelet distribution width (PDW), neutrophil, lymphocyte, monocyte, and platelet counts were extracted from medical records and inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA). Multivariable logistic regression analysis was performed to evaluate the association between inflammatory markers and NAFLD. We also used receiver operating characteristic curve analysis to assess the discriminative ability of inflammatory cytokines for NAFLD.ResultsTwo hundred and sixty-seven obese children were enrolled, including 176 NAFLD patients and 91 simple obesity controls. Multivariable logistic model indicated that increased interleukin (IL)-1β [odds ratio (OR) = 1.15, 95% confidence interval (CI): 1.04-1.27], IL-6 (OR = 1.28, 95% CI: 1.07-1.53), and IL-17 (OR = 1.04, 95% CI: 1.02-1.07) levels were significantly associated with NAFLD. In contrast, we observed non-significant associations for IL-8, IL-12, IL-21, IL-32, tumor necrosis factor-α (TNF-α), neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), lymphocyte to monocyte ratio (LMR), mean platelet volume (MPV), and platelet distribution width (PDW) with NAFLD. The area under the curves (AUCs) of IL-1β, IL-6, and IL-17 to discriminate obese children with or without NAFLD were 0.94, 0.94, and 0.97, respectively.ConclusionsOur results indicated that IL-1β, IL-6, and IL-17 levels were significantly associated with NAFLD. These inflammatory cytokines may serve as non-invasive markers to determine the development of NAFLD and potentially identify additional avenues for therapeutic intervention.
| S-EPMC9751435 | biostudies-literature