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Insulin resistance and adipose tissue interactions as the cornerstone of metabolic(dysfunction)-associated fatty liver disease pathogenesis

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World Journal of Gastroenterology 2023年第25期29卷 3999-4008页

作者： Shreya C Pal Nahum Méndez-Sánchez Faculty of Medicine National Autonomous University of MexicoMexico City 04510Mexico Liver Research Unit Medica Sur Clinic&FoundationMexico City 04510Mexico

The relationship between metabolic derangements and fatty liver development are undeniable,since more than 75% of patients with type 2 diabetes mellitus present with fatty liver.There is also significant epidemiological association between insulin resistance(IR)and metabolic(dysfunction)-associated fatty liver disease(MAFLD).For little more than 2 years,the nomenclature of fatty liver of non-alcoholic origin has been intended to change to MAFLD by multiple groups.While a myriad of reasons for which MAFLD is thought to be of metabolic origin could be exposed,the bottom line relies on the role of IR as an initiator and perpetuator of this disease.There is a reciprocal role in MAFLD development and IR as well as serum glucose concentrations,where increased circulating glucose and insulin result in increased de novo lipogenesis by sterol regulatory elementbinding protein-1c induced lipogenic enzyme stimulation;therefore,increased endogenous production of triglycerides.The same effect is achieved through impaired suppression of adipose tissue(AT)lipolysis in insulin-resistant states,increasing fatty acid influx into the liver.The complementary reciprocal situation occurs when liver steatosis alters hepatokine secretion,modifying fatty acid metabolism as well as IR in a variety of tissues,including skeletal muscle,AT,and the liver.The aim of this review is to discuss the importance of IR and AT interactions in metabolic altered states as perhaps the most important factor in MAFLD pathogenesis.

关键词： Metabolic(dysfunction)-associated fatty liver disease Insulin resistance Adipose tissue Fatty liver Metabolic syndrome adipokine

Liver-adipose tissue crosstalk in alcohol-associated liver disease: The role of mTOR

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Liver Research 2022年第4期6卷 227-237页

作者： Yssa Rodriguez Jack Dunfield Tyson Roderique Hong-Min Ni Department of Pharmacology Toxicology and TherapeuticsUniversity of Kansas Medical CenterKansas CityKSUSA

Background:Alcohol-associated liver disease(ALD)is a major chronic liver disease around the world without successful treatment.Acute alcoholic hepatitis is one of the most severe forms of ALD with high mortality,which is often associated with binge drinking.Alcohol drinking dysregulates lipid metabolism,increases adipose tissue lipolysis,and induces liver steatosis and adipose tissue atrophy.Increasing ev-idence implicates that crosstalk of liver and adipose tissue in the pathogenesis of ALD.Mechanistic target of rapamycin(mTOR)is a phosphatidylinositol 3-kinase(PI3K)-like serine/threonine protein kinase that regulates lipid metabolism,cell proliferation and autophagy.However,the role of mTOR in regulating adipose-liver crosstalk in binge drinking-induced organ damage remains unclear.Methods:We generated liver-specific and adipocyte-specific regulatory-associated protein of mTOR(Rptor)knockout(Rptor LKO and Rptor AKO)as well as Mtor knockout(Mtor LKO and Mtor AKO)mice,by crossing Rptor flox and Mtor flox mice with albumin Cre or adiponectin Cre mice,respectively.In addition,we generated liver and adipocyte double deletion of Rptor or Mtor(Mtor LAKO and Rptor LAKO)mice.The knockout mice with their matched wild-type littermates(Rptor WT and Mtor WT)were subjected to acute gavage of 7 g/kg ethanol.Results:Mice with adipocyte deletion of Rptor or Mtor developed hepatomegaly and adipose tissue at-rophy.Alcohol gavage increased liver injury,hepatic steatosis and inflammation in mouse livers as demonstrated by elevated serum alanine aminotransferase activities,increased hepatic levels of tri-glyceride and increased hepatic numbers of CD68 positive macrophages in mouse livers after alcohol gavage.Liver injury was further exacerbated by deletion of adipocyte Rptor or Mtor.Serum adipokine array analysis revealed that increased levels of pro-inflammatory cytokines IL-6 and TNF a as well as chemokine MCP-1 following acute alcohol gavage in wild-type mice,which were further increased in adipocyte-specific Mtor or Rptor knocko

关键词： Alcohol-associated liver disease(ALD) Liver injury Mechanistic target of rapamycin(mTOR) Adipose atrophy adipokine Liver-adipose tissue crosstalk

Serum omentin-1 is correlated with the severity of liver disease in patients with chronic hepatitis C

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World Journal of Hepatology 2023年第12期15卷 1315-1324页

作者： Georg Peschel Kilian Weigand Jonathan Grimm Martina Müller Christa Buechler Department of Internal Medicine I University Hospital RegensburgRegensburg 93053Germany Department of Internal Medicine Klinikum FürstenfeldbruckFürstenfeldbruck 82256Germany Department of Gastroenterology Gemeinschaftsklinikum MittelrheinKoblenz 56073Germany

BACKGROUND Patients with chronic hepatitis C virus(HCV)infection have increased serum omentin-1.Omentin-1 is an anti-inflammatory adipokine,and higher levels may be a direct effect of HCV infection.Successful elimination of HCV by direct acting antivirals almost normalized circulating levels of various molecules with a role in inflammation.AIM To evaluate the effect of HCV infection on serum omentin-1,serum omentin-1 levels of HCV patients were measured before therapy and at 12 wk after therapy end.Associations of serum omentin-1 with parameters of inflammation and liver function were explored at both time points.Serum omentin-1 levels of patients with and without liver cirrhosis,which was defined by ultrasound or the fibrosis-4(FIB-4)score,were compared.METHODS Serum omentin-1 levels were measured by enzyme-linked immunosorbent assay in 84 chronic HCV patients before therapy and at 12 wk after therapy end where sustained virological response 12(SVR12)was achieved in all patients.Serum omentin-1 of 14 non-infected controls was measured in parallel.RESULTS In patients with chronic HCV,serum omentin-1 levels were not related to viral load or viral genotype.HCV patients with liver steatosis and HCV patients with diabetes had serum omentin-1 levels comparable to patients not suffering from these conditions.Serum omentin-1 levels at SVR12 were similar in comparison to pretreatment levels.In addition,serum levels did not differ between HCV-infected patients and non-infected controls.Serum omentin-1 levels did not correlate with leukocyte count or C-reactive protein.Positive correlations of serum omentin-1 with bilirubin and the model for end-stage liver disease score(MELD)were detected before therapy and at SVR12 in the whole cohort.Bilirubin and the MELD score also positively correlated with serum omentin-1 levels in the subgroup of patients with ultrasound diagnosed liver cirrhosis before therapy.At SVR12,serum omentin-1 levels of patients with liver cirrhosis negatively correlated with albumin.Before therapy start,p

关键词： Direct acting antivirals Hepatitis C Liver cirrhosis adipokine

Abnormal adipokines Associated with Various Types of Obesity in Chinese Children and Adolescents

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Biomedical and Environmental Sciences 2011年第1期24卷 12-21页

作者： ZHANG MeiXian ZHAO XiaoYuan LIMing CHENG Hong HOU DongQing WEN Yu Katherine CIANFLONE MI Jie Department of Epidemiology Capital Institute of Pediatrics Beijing 100020 China Department of Endocrinology Peking Union Medical College Hospital Peking Union Medical College and ChineseAcademy of Medical Sciences Beijing 100730 China Department of Pediatrics Tongji HospitalHuaZhong University of Science and Technology Wuhan 430030 Hubei China Centre de Recherche Institut Universitaire de Cardiologie et Pneumologie de Quebec Universite Laval Quebec Canada

Objective To explore the role of adipokines including insulin, resistin, leptin, adiponectin, acylation stimulating protein （ASP） and complement C3 （C3） in various types of obesity （peripheral obesity, abdominal obesity and mixed obesity） in Chinese children and adolescents, and their relationships with body size and pubertal development. Methods Children and adolescents （n=3 508） aged 6 to 18 years, with 1 788 boys and 1 720 girls were assessed for body mass index, waist circumference, pubertal development, blood insulin, resistin, leptin, adiponectin, ASP and C3 levels. Three types of obesity [peripheral obesity （n=43）, abdominal obesity （n=473）, mixed obesity （n=1 187）] and non‐obese control （n=1 805） were defined with combined use of Chinese body mass index and waist circumference criteria. Results Serum resistin, leptin and adiponectin levels were higher in girls than those in boys （all P0.01）. Insulin and leptin increased and adiponectin decreased across five Tanner stages in both girls and boys （all P0.001）, while ASP changed only in girls （P0.001） and C3 only in boys （P0.001）. Insulin, leptin and ASP were higher, but adiponectin was lower in all three types of obesity vs. the non‐obese control （all P0.05）. The greatest abnormalities of all six adipokines were found in the mixed obesity group. With inclusion of body mass index and waist circumference in simultaneous regression analyses, both body size indices were independently and significantly correlated with insulin, leptin and adiponectin after age and gender adjustment. Compared with waist circumference, the body mass index was stronger in interpreting insulin, leptin, adiponectin and ASP levels, whereas it was weaker in explaining variance of plasma C3. Conclusions Obese children have a worse metabolic profile with high insulin, resistin, leptin, ASP and C3, and low adiponectin levels. The adipokine profile in mixed obesity is worse than that in peripheral or abdominal obesity. Identification of obese subjects with a malignant adipokine profile using

关键词： adipokine Types of obesity Body mass index Waist circumference Child and adolescent Chinese

Leptin in hepatocellular carcinoma

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World Journal of Gastroenterology 2010年第46期16卷 5801-5809页

作者： Shen-Nien Wang King Teh Lee Chen-Guo Ker Division of Hepatobiliary Surgery Department of SurgeryKaohsiung Medical University Hospital Department of Surgery Faculty of MedicineCollege of MedicineKaohsiung Medical University Cancer Center Department of SurgeryKaohsiung Medical University Hospital Department of Surgery Kaohsiung Municipal Hsiao-Kang Hospital Graduate Institute of Medicine College of MedicineKaohsiung Medical University

The risk factors for hepatocellular carcinoma (HCC) development have been established,and include chronic hepatitis B and C,heavy alcohol consumption,and aflatoxins.In fact,5%-30% of patients with HCC still lack a readily identifiable risk factor.It has been reported that the majority of "cryptogenic" HCC may be attributed to nonalcoholic fatty liver disease,the hepatic presentation of the metabolic syndrome (MS).Obesity is associated with the development of the MS.Recently,adipose tissue has been considered as an endocrine organ because of its capacity to secrete a variety of cytokines,which are collectively known as the adipokines.Leptin,the product of the obese gene,is mainly produced by adipose tissue.Since leptin was first characterized in 1994,accumulated literature has demonstrated the involvement of this adipokine in several areas of human physiology.After binding to its receptor,leptin initiates a cascade of signaling events and subsequent cellular effects.In addition to being the regulatory mediator of energy homeostasis,several in vitro studies have demonstrated the fibrogenic role of leptin in the liver.Furthermore,the deregulated expression of leptin and its receptor have been demonstrated to be associated with a variety of metabolic disorders as well as human cancers.Most importantly,direct evidence supporting the inhibitory and/or activating role of leptin in the process of carcinogenesis and progression of human HCC has been accumulating rapidly.This review aims to provide important insights into the potential mechanisms of leptin in the development of HCC.Hopefully,further investigations will shed light on a new therapeutic target in HCC.

关键词： adipokine Hepatocellular carcinoma Leptin Liver cirrhosis Metabolic syndrome Obesity Steatohepatitis

Exogenous phosphatidic acid reduces acetaminophen-induced liver injury in mice by activating hepatic interleukin-6 signaling through inter-organ crosstalk

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Acta Pharmaceutica Sinica B 2021年第12期11卷 3836-3846页

作者： Melissa M.Clemens Stefanie Kennon-McGill Joel H.Vazquez Owen W.Stephens Erich A.Peterson Donald J.Johann Felicia D.Allard Eric U.Yee Sandra SMcCullough Laura P.James Brian N.Finck Mitchell R.McGill Department of Pharmacology and Toxicology College of MedicineUniversity of Arkansas for Medical SciencesLittle RockAR 72205USA Interdisciplinary Graduate Program in Biomedical Sciences Graduate SchoolUniversity of Arkansas for Medical SciencesLittle RockAR 72205USA Department of Environmental and Occupational Health Fay W.Boozman College of Public HealthUniversity of Arkansas for Medical SciencesLittle RockAR 72205USA Winthrop P.Rockefeller Cancer Institute University of Arkansas for Medical SciencesLittle RockAR 72205USA Department of Pathology Renaissance School of MedicineStony Brook UniversityStony BrookNY 11794USA Department of Pediatrics College of MedicineUniversity of Arkansas for Medical SciencesLittle RockAR2205USA Division of Geriatrics and Nutritional Sciences Department of Internal MedicineWashington University School of MedicineSt.LouisMO 63110USA Center for Dietary Supplement Research University of Arkansas for Medical SciencesLittle RockAR 72205USA

We previously demonstrated that endogenous phosphatidic acid(PA)promotes liver regeneration after acetaminophen(APAP)hepatotoxicity.Here,we hypothesized that exogenous PA is also beneficial.To test that,we treated mice with a toxic APAP dose at 0 h,followed by PA or vehicle(Veh)posttreatment.We then collected blood and liver at 6,24,and 52 h.Post-treatment with PA 2 h after APAP protected against liver injury at 6 h,and the combination of PA and N-acetyl-L-cysteine(NAC)reduced injury more than NAC alone.Interestingly,PA did not affect canonical mechanisms of APAP toxicity.Instead,transcriptomics revealed that PA activated interleukin-6(IL-6)signaling in the liver.Consistent with that,serum IL-6 and hepatic signal transducer and activator of transcription 3(Stat3)phosphorylation increased in PA-treated mice.Furthermore,PA failed to protect against APAP in IL-6-deficient animals.Interestingly,IL-6 expression increased 18-fold in adipose tissue after PA,indicating that adipose is a source of PA-induced circulating IL-6.Surprisingly,however,exogenous PA did not alter regeneration,despite the importance of endogenous PA in liver repair,possibly due to its short half-life.These data demonstrate that exogenous PA is also beneficial in APAP toxicity and reinforce the protective effects of IL-6 in this model.

关键词： Acute liver injury Acute liver failure adipokine Cytokine Dietary supplement Drug-induced liver injury Hepatotoxicity Lipid

Increased asprosin is associated with non-alcoholic fatty liver disease in children with obesity

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World Journal of Pediatrics 2021年第4期17卷 394-399页

作者： Lu-Jie Liu Yu-Rong Kang Yan-Feng Xiao Department of Pediatrics The Second Affiliated Hospital of Xi’an Jiaotong University157 Xiwu RoadXi’an 710061China

Background Obesity is a common disease among children,often accompanied by a lot of metabolic disease.Non-alcoholic fatty liver disease(NAFLD)is one of the most common complications of obesity among children and adolescents.Asprosin has been identified as a new adipokine that is closely associated with hepatic glucose metabolism.However,few data on asprosin in obese children with NAFLD are available.The present study focuses on the relationship between serum asprosin level and NAFLD in children with obesity.Methods A total of 110 subjects(71 boys and 39 girls aged 6–18 years)were recruited from the Second Affiliated Hospital of Xi’an Jiaotong University:36 obese children with NAFLD,39 obese children without NAFLD and 35 lean controls.Anthropometric parameters and biochemical data were measured,and the concentrations of asprosin were detected by ELISA.Results The levels of serum asprosin were significantly higher in obese children,particularly those with NAFLD and were positively correlated with body mass index,waist to height ratio,fasting blood glucose,alanine aminotransferase and tumor necrosis factor-alpha.Furthermore,asprosin was independently associated with NAFLD in binary logistic regression analysis.Conclusion Serum asprosin levels were elevated in obese children,especially in those with NAFLD,and were involved in the pathogenesis of NAFLD in children with obesity.

关键词： adipokine Asprosin Non-alcoholic fatty liver disease Obesity

Serum omentin and vaspin levels in cirrhotic patients with and without portal vein thrombosis

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World Journal of Gastroenterology 2017年第14期23卷 2613-2624页

作者： Michal Kukla Marek Waluga Michal Zorniak Agnieszka Berdowska Piotr Wosiewicz Tomasz Sawczyn Rafal J Buldak Marek Ochman Katarzyna Ziora Tadeusz Krzemiński Marek Hartleb Department of Gastroenterology and Hepatology Medical University of Silesia in Katowice Department of Microbiology and Biotechnology Jan Dlugosz University Department of Physiology Medical University of Silesia in Katowice Department of Biochemistry in Zabrze Medical University of Silesia in Katowice Department of Cardiac Surgery and Transplantation Silesian Center for Heart Diseases Department of Pediatrics Medical University of Silesia in Katowice Department of Pharmacology Medical University of Silesia in Katowice

AIM To investigate serum omentin and vaspin levels in cirrhotic patients; and to assess the relationship of these levels with hemostatic parameters, metabolic abnormalities, cirrhosis severity and etiology.METHODS Fifty-one cirrhotic patients(17 with portal vein thrombosis) were analyzed. Serum omentin and vaspin levels were measured with commercially available direct enzyme-linked immunosorbent assays(ELISAs). To assess platelet activity, the following tests were performed using a MULTIPLATE?PLATELET FUNCTION ANALYZER:(1) an ADP-induced platelet activation test;(2) a cyclooxygenase dependent aggregation test(ASPI test);(3) a von Willebrand factor and glycoprotein Ibdependent aggregation(using ristocetin) test(RISTO test); and(4) a test for thrombin receptor-activating peptide-6 induced activation of the thrombin receptor, which is sensitive to Ⅱb/Ⅲa receptor antagonists. RESULTS Omentin, but not vaspin, serum concentrations were significantly decreased in patients with portal vein thrombosis(PVT)(P = 0.01). Prothrombin levels were significantly increased in patients with PVT(P = 0.01). The thrombin receptor activating peptide(TRAP) test results were significantly lower in the PVT group(P = 0.03). No significant differences in adipokines serum levels were found regarding the etiology or severity of liver cirrhosis assessed according to the Child-Pugh or Model of End-Stage Liver Disease(MELD) scores. There was a significant increase in the TRAP(P = 0.03), ASPI(P = 0.001) and RISTO high-test(P = 0.02) results in patients with lower MELD scores. Serum omentin and vaspin levels were significantly down-regulated in patients without insulin resistance(P = 0.03, P = 0.02, respectively). A positive relationship between omentin and vaspin levels were found both when all of the patients were analyzed(r = 0.41, P = 0.01) and among those with PVT(r = 0.94, P < 0.001).CONCLUSION Serum omentin levels are increased in patients without PVT. Cirrhosis origin and grade do not affect omentin and vaspin levels. The analyzed adipokin

关键词： Omentin Vaspin 肝硬化 adipokine 门静脉血栓门高血压

adipokine在肥胖症及胰岛素抵抗中的作用(综述)

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河北科技师范学院学报 2011年第2期25卷 75-80页

作者：李娟沈飞陈巍燕山大学体育学院河北秦皇岛066004 河北科技师范学院体育系

从adipokines与胰岛素抵抗的关系,adipokines与肥胖者脂肪组织巨噬细胞浸润,炎症与胰岛素抵抗信号转导,内质网应激与胰岛素抵抗等方面综述了adipokines在肥胖症及胰岛素抵抗中的作用;并着重探讨了肥胖,adipokines,炎症,胰岛素抵抗四者... 详细信息

从adipokines与胰岛素抵抗的关系,adipokines与肥胖者脂肪组织巨噬细胞浸润,炎症与胰岛素抵抗信号转导,内质网应激与胰岛素抵抗等方面综述了adipokines在肥胖症及胰岛素抵抗中的作用;并着重探讨了肥胖,adipokines,炎症,胰岛素抵抗四者之间的关系。

关键词： adipokine 肥胖症胰岛素抵抗