• MASLD
• Oesophageal varices
• carvedilol
• portal hypertension

• ACE, angiotensin-converting enzyme
• ACE-I, angiotensin-converting enzyme inhibitor
• AKI, acute kidney injury
• ALM, appendicular lean mass
• ARB, angiotensin receptor blocker
• ASM, appendicular skeletal mass
• AT1R, angiotensin type 1 receptor
• AT2R, angiotensin type 2 receptor
• ATP, adenosine-5′-triphosphate
• AWGS, Asian Working Group for Sarcopenia
• BCAA, branched chained amino acids
• BIA, bioelectrical impedance analysis
• BMI, body mass index
• CART, classification and regression tree
• CKD, chronic kidney disease
• CRP, C-reactive protein
• DEXA, dual energy X-ray absorptiometry
• EAA, essential amino acids
• ESPEN-SIG, European Society for Clinical Nutrition and Metabolism Special Interests Groups
• ESRD, end-stage renal disease
• EWGSOP, European Working Group on Sarcopenia in Older People
• FAD, flavin adenine dinucleotide
• FADH2, flavin adenine dinucleotide +2 hydrogen
• FNIH, Foundation for the National Institutes of Health
• GTP, guanosine-5′-triphosphate
• GnRH, gonadotrophin-releasing hormone
• HCC, hepatocellular carcinoma
• HPT, hypothalamic-pituitary-testicular
• IFN-γ, interferon γ
• IGF-1, insulin-like growth factor 1
• IL-1, interleukin-1
• IL-6, interleukin-6
• IWGS, International Working Group on Sarcopenia
• LH, luteinizing hormone
• MELD, Model for End-Stage Liver Disease
• MuRF1, muscle RING-finger-1
• NAD, nicotinamide adenine dinucleotide
• NADH, nicotinamide adenine dinucleotide + hydrogen
• NADPH, nicotinamide adenine dinucleotide phosphate
• NAFLD, non-alcoholic fatty liver disease
• NASH, non-alcoholic steatohepatitis
• NF-κβ, nuclear factor κβ
• NHANES, National Health and Nutritional Examination Survey
• PMI, psoas muscle index
• PMTH, psoas muscle thickness
• RAAS, renin-angiotensin-aldosterone system
• ROS, reactive oxygen species
• SARC-F, Strength, Assistance with walking, Rise from a chair, Climb stairs, and Falls
• SHBG, sex hormone binding globulin
• SMI, skeletal muscle index
• SNS, sympathetic nervous system
• SPPB, Short Performance Physical Battery
• TNF-α, tumor necrosis factor α
• UCSF, University of California, San Francisco
• UNOS, United Network of Organ Sharing
• cirrhosis
• energy
• mTOR, mammalian target of rapamycin
• metabolism
• muscle
• sarcopenia

• Cirrhosis
• Diabetes
• Glucose intolerance
• Hepatogenous diabetes
• Insulin resistance
• Metabolism

To investigate the short-term dynamic changes and the factors associated with regression of glucose metabolism disorders in patients with hepatitis flare of chronic hepatitis B virus (HBV) infection.

In this study, 118 patients with severe hepatitis flare of chronic HBV infection were prospectively studied. Oral glucose tolerance test was performed on admission and during follow-up to evaluate dynamic changes in glucose metabolism disorders. The factors associated with regression of glucose metabolism disorders were identified using univariate and multivariate logistic regression analyses.

The prevalence of diabetes was significantly higher in 70 (47.1%) patients with liver cirrhosis than that in 48 (16.8%) patients without liver cirrhosis. The prevalence of impaired glucose tolerance in patients with liver cirrhosis (35.7%) was significantly lower than that in patients without liver cirrhosis (47.8%). After a follow-up of 20.0 ± 18.7 days, 28 of 31 (90.3%) patients without liver cirrhosis experienced regression of glucose metabolism disorders. Additionally, 30 (54.5%) patients with liver cirrhosis experienced regression of glucose metabolism disorders after 42.0 ± 36.2 days. In patients with liver cirrhosis, those with regression of glucose metabolism disorders had significantly higher levels of homeostasis model assessment-β-cell function, albumin (ALB), and a significantly lower level of fibrosis-4 score. ALB was identified as an independent factor associated with the regression of glucose metabolism disorders in patients with liver cirrhosis.

Severe acute liver inflammation aggravates glucose metabolism disorders in patients with hepatitis B-related liver cirrhosis and high ALB level is associated with regression of glucose metabolism disorders upon resolution of acute liver inflammation.

• Albumins
• Diabetes Mellitus
• Hepatitis B/complications
• Hepatitis B virus
• Hepatitis B, Chronic/complications
• Humans
• Inflammation/complications
• Liver Cirrhosis/complications
• Liver Cirrhosis/metabolism
• Symptom Flare Up

• ammonia
• decompensated cirrhosis
• hepatic fibrosis
• moderate exercise
• portal hypertension

• Animals
• Caloric Restriction
• Carbon Tetrachloride
• Chemical and Drug Induced Liver Injury/etiology
• Chemical and Drug Induced Liver Injury/metabolism
• Chemical and Drug Induced Liver Injury/pathology
• Chemical and Drug Induced Liver Injury/therapy
• Energy Intake
• Exercise Therapy
• Healthy Lifestyle
• Hypertension, Portal/chemically induced
• Hypertension, Portal/metabolism
• Hypertension, Portal/physiopathology
• Hypertension, Portal/therapy
• Liver/metabolism
• Liver/pathology
• Liver Cirrhosis, Experimental/chemically induced
• Liver Cirrhosis, Experimental/metabolism
• Liver Cirrhosis, Experimental/pathology
• Liver Cirrhosis, Experimental/therapy
• Male
• Physical Endurance
• Rats, Wistar
• Risk Reduction Behavior
• Thioacetamide
• Time Factors
• Rats

• accident & emergency medicine
• clinical pharmacology
• gastroenterology
• general endocrinology
• internal medicine
• therapeutics

• Aged
• Aged, 80 and over
• Cohort Studies
• End Stage Liver Disease
• Glucose
• Humans
• Hyperkalemia/drug therapy
• Insulin
• Liver Cirrhosis/complications
• Liver Cirrhosis/drug therapy
• Middle Aged
• Retrospective Studies
• Severity of Illness Index

• Acute-on-chronic liver failure
• Diabetes
• Hepatitis B virus
• Hepatogenous diabetes
• Hypoglycemia
• Impaired glucose tolerance
• Oral glucose tolerance test
• Prognosis
• Stress-induced hyperglycemia
• β-Cell function

We investigated the impact of postreperfusion syndrome (PRS) on hyperglycemia occurrence and connecting (C) peptide release, which acts as a surrogate marker for insulin resistance, during the intraoperative period after graft reperfusion in patients undergoing living donor liver transplantation (LDLT) using propensity score (PS)-matching analysis.

Medical records from 324 adult patients who underwent elective LDLT were retrospectively reviewed, and their data were analyzed according to PRS occurrence (PRS vs. non-PRS groups) using the PS-matching method. Intraoperative levels of blood glucose and C-peptide were measured through the arterial or venous line at each surgical phase. Hyperglycemia was defined as a peak glucose level >200 mg/dL, and normal plasma concentrations of C-peptide in the fasting state were taken to range between 0.5 and 2.0 ng/mL.

After PS matching, there were no significant differences in pre- and intra-operative recipient findings and donor-graft findings between groups. Although glucose and C-peptide levels continuously increased through the surgical phases in both groups, glucose and C-peptide levels during the neohepatic phase were significantly higher in the PRS group than in the non-PRS group, and larger changes in levels were observed between the preanhepatic and neohepatic phases. There were higher incidences of C-peptide levels >2.0 ng/mL and peak glucose levels >200 mg/dL in the neohepatic phase in patients with PRS than in those without. PRS adjusted for PS with or without exogenous insulin infusion was significantly associated with hyperglycemia occurrence during the neohepatic phase.

Elucidating the association between PRS and hyperglycemia occurrence will help with establishing a standard protocol for intraoperative glycemic control in patients undergoing LDLT.

• adiponectin
• insulin resistance
• leptin
• liver cirrhosis

Studies in animal models have suggested that hepatic steatosis impacts on portal pressure, potentially by inducing liver sinusoidal endothelial dysfunction and thereby increasing intrahepatic resistance. Thus, we aimed to evaluate the impact of hepatic steatosis on hepatic venous pressure gradient (HVPG) in patients with chronic liver disease.

261 patients undergoing simultaneous HVPG measurements and controlled attenuation parameter (CAP)-based steatosis assessment were included in this retrospective study.

The majority of patients had cirrhosis (n = 205; 78.5%) and n = 191 (73.2%) had clinically significant portal hypertension (CSPH; HVPG≥10mmHg). Hepatic steatosis (S1/2/3; CAP ≥248dB/m) was present in n = 102 (39.1%). Overall, HVPG was comparable between patients with vs. without hepatic steatosis (15.5±7.5 vs. 14.8±7.7mmHg; p = 0.465). Neither in patients with HVPG (<6mmHg; p = 0.371) nor in patients with mild portal hypertension (HVPG 6–9mmHg; p = 0.716) or CSPH (HVPG≥10mmHg; p = 0.311) any correlation between CAP and HVPG was found. Interestingly, in patients with liver fibrosis F2/3, there was a negative correlation between CAP and HVPG (Pearson’s ρ:-0.522; p≤0.001). In multivariate analysis, higher CAP was an independent ‘protective’ factor for the presence of CSPH (odds ratio [OR] per 10dB/m: 0.92, 95% confidence interval [CI]:0.85–1.00; p = 0.045), while liver stiffness was associated with the presence of CSPH (OR per kPa: 1.26, 95%CI: 1.17–1.36; p≤0.001). In 78 patients, in whom liver biopsy was performed, HVPG was neither correlated with percentage of histological steatosis (p = 0.714) nor with histological steatosis grade (p = 0.957).

Hepatic steatosis, as assessed by CAP and liver histology, did not impact on HVPG in our cohort comprising a high proportion of patients with advanced chronic liver disease. However, high CAP values (i.e. pronounced hepatic steatosis) might lead to overestimation of liver fibrosis by ‘artificially’ increasing transient elastography-based liver stiffness measurements.

• advanced chronic liver disease
• body composition
• computed tomography
• portal hypertension

• Endothelial dysfunction
• Insulin resistance
• Metabolic syndrome
• Non-alcoholic fatty liver disease

• Animals
• Disease Models, Animal
• Endothelial Cells/enzymology
• Endothelium, Vascular/cytology
• Endothelium, Vascular/enzymology
• Endothelium, Vascular/physiopathology
• Humans
• Insulin/metabolism
• Liver/blood supply
• Liver/pathology
• Metabolic Syndrome/complications
• Metabolic Syndrome/pathology
• Microvessels/cytology
• Microvessels/physiopathology
• Nitric Oxide/metabolism
• Nitric Oxide Synthase/metabolism
• Non-alcoholic Fatty Liver Disease/etiology
• Non-alcoholic Fatty Liver Disease/pathology
• Oxidative Stress
• Vasodilation

• Insulin resistance
• cirrhosis
• diabetes
• portal hemodynamics

• Hyperinsulinaemia
• diabetes
• hepatic schistosomiasis japonica
• insulin resistance
• portosystemic shunts

• 2-h plasma glucose
• Hepatic decompensation
• Insulin resistance
• Overall survival
• Type 2 diabetes

• Aged
• Blood Glucose/metabolism
• Cohort Studies
• Diabetes Mellitus, Type 2/complications
• Diabetes Mellitus, Type 2/metabolism
• Disease Progression
• Female
• Glucose Tolerance Test
• Hepatitis C, Chronic/complications
• Hepatitis C, Chronic/metabolism
• Humans
• Insulin Resistance
• Liver Cirrhosis/complications
• Liver Cirrhosis/metabolism
• Liver Cirrhosis/mortality
• Liver Failure/etiology
• Liver Failure/metabolism
• Liver Failure/mortality
• Liver Failure/surgery
• Liver Transplantation
• Longitudinal Studies
• Male
• Middle Aged
• Prognosis
• Proportional Hazards Models
• Prospective Studies
• Survival Rate

AIM: To investigate the plasma levels of betatrophin in patients with cirrhosis.

METHODS: Forty patients diagnosed at the clinic with liver cirrhosis according to biological, ultrasonographic, or histological criteria were included. The severity of cirrhosis was classified according to Pugh’s modification of Child’s classification and MELD score. Insulin resistance (IR) was assessed by the Homeostasis Model Assessment. A total of 20 patients showed a MELD score higher than 14. The control group consisted in 15 sex-and aged-matched subjects. Fasting blood samples were obtained for subsequent analysis. Serum insulin was determined by Liaison automated immune chemiluminiscence assay (DiaSorin S.p.A.) using a sandwich assay. The sensitivity of the assay was 0.2 μU/mL. The intra and interassay variation coefficients were < 4% and < 10%, respectively. The normal values were between 2 and 17 μU/mL. Human active betatrophin was analyzed by specific quantitative sandwich ELISA (Aviscera Bioscience^®). The sensitivity of the assay was 0.4 ng/mL, and the intra and interassay reproducibility were < 6% and < 10%, respectively.

RESULTS: Plasma betatrophin levels were significantly increased in patients with cirrhosis compared with those in healthy subjects (P = 0.0001). Betatrophin levels were also associated with disease severity, being higher in Child-Pugh C patients compared to Child-Pugh B (P < 0.0005) and in patients who displayed a MELD score higher than 14 points compared to patients with lower punctuation (P = 0.01). In addition, we found a positive correlation between plasma betatrophin levels and the severity of cirrhosis according to Child-Pugh classification (r = 0.53; P < 0.01) or MELD score (r = 0.45; P < 0.01). In the overall cohort, a moderate correlation between serum betatrophin and plasmatic bilirrubin (r = 0.39; P < 0.01) has been observed, as well as an inverse correlation between betatrophin and albumin (r = -0.41; P < 0.01) or prothrombin time (r = -0.44; P <0.01). Moreover, insulin resistance was observed in 82.5% of the cirrhotic patients. In this group of patients, betatrophin levels were significantly higher than those in the group of patients without IR (P < 0.05).

CONCLUSION: Plasma betatrophin is increased in patients with cirrhosis. This increase is related to the severity of cirrhosis, as well as with the emergence of insulin resistance.

• Liver cirrhosis
• Betatrophin
• Insulin resistance
• Betatrophin liver
• Betatrophin insulin

• Adult
• Aged
• Angiopoietin-Like Protein 8
• Angiopoietin-like Proteins
• Enzyme-Linked Immunosorbent Assay
• Female
• Homeostasis
• Humans
• Insulin Resistance
• Liver Cirrhosis/blood
• Liver Cirrhosis/pathology
• Luminescence
• Male
• Middle Aged
• Peptide Hormones/blood
• Reproducibility of Results
• Retrospective Studies
• Severity of Illness Index

• chronic disease
• glucose transporter
• human
• liver
• vascular adhesion protein-1

• autosomal recessive polycystic kidney disease
• new-onset diabetes after transplantation
• pediatrics
• renal transplant

• Body mass index
• Chronic liver disease
• Enfermedad hepática crónica
• GPVH
• HOMA
• HVPG
• Varices
• Índice de masa corporal

AIM: To determine the potential role of type 2 diabetes mellitus (DM) in the progression of chronic hepatitis B (CHB) to cirrhosis in Chinese patients.

METHODS: A total of 292 patients with CHB and/or CHB-related cirrhosis treated at the China-Japan Friendship Hospital and Sichuan Science City Hospital from January 2007 to December 2011 were studied. Demographic, clinical, biochemical, and metabolic features/data were analyzed and multivariate logistic regression model was used to determine the role of type 2 DM in the progression of CHB to cirrhosis.

RESULTS: Of the 292 patients, 91 were diagnosed with simple CHB and 201 with CHB-related cirrhosis. Seventy-eight patients were diagnosed with type 2 DM, including 10 in the CHB group and 68 in the cirrhosis group (11.0% vs 33.8%, P < 0.001). In the multivariate analysis, compared with patients with simple CHB, after controlled by gender, age, body mass index (weight), smoking, drinking and Child score, type-2 DM was shown to be an independent risk factor for CHB-related cirrhosis (odds ratio, 4.434, 95% confidence interval, 2.049-9.591, P < 0.001).

CONCLUSION: Our findings suggest that type 2 DM may play an important role in the progression of CHB to cirrhosis and may be a newly identified risk factor for CHB-related cirrhosis.

• Type 2 diabetes mellitus
• Chronic hepatitis B
• Cirrhosis