Significant correlations between severe fatty liver and risk factors for metabolic syndrome

Hsiao, Pi‐Jung; Kuo, Kung‐Kai; Shin, Shyi–Jang; Yang, Yoona; Lin, Wen‐Yi; Yang, Jeng‐Fu; Chiu, Chaw-Chi; Chuang, Wan‐Long; Tsai, Tsung-Yu; Yu, Ming‐Lung

doi:10.1111/j.1440-1746.2006.04698.x

Cited by 127 publications

(90 citation statements)

References 48 publications

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“…In the present study, the presence of LS on abdominal ultrasound was associated with fasting insulin and total cholesterol, similar to fi ndings previously reported by other authors in non-HBV patients 25,[27][28][29] , indicating that LS is related to disordered metabolism of blood glucose and lipids. Although BMI data were available only in a small subset of patients (n = 19), these data revealed a signifi cant difference between the two study groups.…”

Section: Discussionsupporting

confidence: 80%

Clinical and laboratory characteristics associated with dyslipidemia and liver steatosis in chronic HBV carriers

Nau

Soares

Shiozawa

et al. 2014

Rev. Soc. Bras. Med. Trop.

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Section: Discussionsupporting

confidence: 80%

Clinical and laboratory characteristics associated with dyslipidemia and liver steatosis in chronic HBV carriers

Nau

Soares

Shiozawa

et al. 2014

Rev. Soc. Bras. Med. Trop.

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“…This finding indicates that not only was basal gluconeogenesis reduced in the HFD-fed siTORC2 mice, but hepatic insulin sensitivity was also improved in these mice. Hepatic steatosis is a characteristic feature of HFD-fed mice and other insulin-resistant/diabetic states (13,24,25), and, this abnormality was prevented in HFD-fed siTORC2 mice (Fig. 4E).…”

Section: Glucose Homeostasis and Insulin Sensitivity In Torc2 Sirna-tmentioning

confidence: 97%

Novel liver-specific TORC2 siRNA corrects hyperglycemia in rodent models of type 2 diabetes

Saberi

Bjelica

Schenk

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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[transducer of regulated cAMP-responsive element-binding protein (CREB) activity 2] is a major regulator of hepatic gluconeogenesis and is increased in hyperglycemic rodent models. Because chronic hyperglycemia and increased hepatic glucose production, via increased gluconeogenesis, is a key feature of type 2 diabetes, an effective in vivo method to efficiently knock down TORC2 could provide a potential therapy for treating hyperglycemia and type 2 diabetes. To assess this, primary mouse hepatocytes, high-fat diet (HFD)-fed mice, and Zucker diabetic fatty (ZDF) rats were treated with a siRNA against TORC2 (siTORC2), which was delivered via a novel lipid nanoparticle system, or control siRNA (siCON). Compared with siCON, administration of siTORC2 resulted in highly efficient, sustained (1-3 wk) knockdown of TORC2 and its gluconeogenic target genes phosphoenolpyruvate carboxykinase and glucose-6-phophatase in primary mouse hepatocytes and in the livers of HFD-fed mice. In mice, this knockdown was specific to the liver and did not occur in kidney, skeletal muscle, or adipose tissue. In HFD-fed mice, siTORC2 reduced in vivo gluconeogenic capacity, fasting hepatic glucose production, and hyperglycemia, and led to improved hepatic and skeletal muscle insulin sensitivity. siTORC2 treatment also improved systemic hyperglycemia in ZDF rats. In conclusion, these results demonstrate the importance of TORC2 in modulating HGP in vivo and highlight a novel, liver-specific siRNA approach for the potential treatment of hyperglycemia and type 2 diabetes.transducer of regulated cAMP-responsive element-binding protein activity 2; diabetes; small interfering RNA IN PATIENTS WITH TYPE 2 DIABETES, increased glucose output from the liver is a major cause of fasting hyperglycemia (5,15,20,22,26), and, consistent with this idea, the degree of fasting hyperglycemia is positively correlated to the magnitude of the increase in hepatic glucose production (HGP) (5,15,20,33). Hepatic gluconeogenesis is a key component of HGP (30), and studies in fasted individuals using magnetic resonance spectroscopy and isotope dilution-based techniques suggest that increased gluconeogenesis is the major contributor to fasting hyperglycemia in type 2 diabetes (5,22,33). Excessive glucose output from the liver can also contribute to postprandial hyperglycemia (22, 30), which is due to a reduced ability of insulin to suppress HGP as well as impaired insulin-stimulated glucose uptake in insulin sensitive tissues (15,26).The cAMP-responsive element-binding protein (CREB) is a major positive transcriptional regulator of the gluconeogenic gene program (11). The ability of CREB to induce gluconeogenesis is dependent on the recently identified CREB coactivator transducer of regulated CREB activity 2 [TORC2, also known as CREB-regulated transcription coactivator 2 (CRTC2)] (3, 7, 8, 16). When hepatic cAMP levels are increased (e.g., by increased glucagon), TORC2 becomes dephosphorylated and translocates to the nucleus, where it coactivates CREB to induce transcripti...

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“…26,27 Hepatic steatosis, even nonalcoholic steatohepatitis (NASH), is a liver disease that occurs in the absence of alcohol abuse and is frequently related to MS and type 2 diabetes. 12 We have previously reported that the severity of hepatic steatosis as assessed by ultrasound (B-mode, 3.5 MHz convex transducer) is significantly correlated with the results of hepatic enzyme tests such as AST, ALT and GGT (Po0.001); 15 however, whether hepatic steatosis can lead to abnormal hepatic enzyme test results remains controversial. [27][28][29] Regarding the relationship between MS and abnormal liver function, Miyatake et al…”

Section: Discussionmentioning

confidence: 99%

Abnormal liver function test results are related to metabolic syndrome and BMI in Taiwanese adults without chronic hepatitis B or C

Hsieh

Hou

et al. 2009

Int J Obes

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Background: Metabolic syndrome (MS) is considered a cause of abnormal deposition of fat into hepatocytes, which might be associated with hepatic steatosis or abnormal liver function. Objective: The aim of this study was to explore the factors associated with MS and the relationship between MS and abnormal aspartate aminotransferase (AST), alanine aminotransferase (ALT) and g-glutamyl transferase (GGT) levels in Taiwanese subjects without chronic hepatitis B (CHB) or C (CHC). Subjects: We enrolled 2539 Taiwanese adults without CHB or CHC (age range: 16-88 years old) and investigated the factors related to MS using the NCEP-ATP (National Cholesterol Education Program-Adult Treatment Panel) III criteria; body mass index (BMI) was measured using Asia-Pacific criteria. Results: The prevalence rate of MS in Taiwanese adults without CHB or CHC was 16.9% using the modified ATP III criteria and 15.4% using the International Diabetes Federation criteria. Males had a significantly higher prevalence rate than females (Po0.001), and subjects with MS were significantly older and had significantly higher BMI values and AST, ALT and GGT levels (all Po0.001). In univariate analyses, the abnormality of liver function test results were related to gender, level of fasting sugar, systolic blood pressure, triglyceride, high-density lipoprotein, BMI and MS (all Po0.05). Multivariate analysis showed that the male gender, a higher BMI value and MS were related to abnormal liver function test results. The cutoff value for ALT in relation to MS is 31 IU l À1 for male and 18 IU l À1 for female.

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Significant correlations between severe fatty liver and risk factors for metabolic syndrome

Cited by 127 publications

References 48 publications

Clinical and laboratory characteristics associated with dyslipidemia and liver steatosis in chronic HBV carriers

Clinical and laboratory characteristics associated with dyslipidemia and liver steatosis in chronic HBV carriers

Novel liver-specific TORC2 siRNA corrects hyperglycemia in rodent models of type 2 diabetes

Abnormal liver function test results are related to metabolic syndrome and BMI in Taiwanese adults without chronic hepatitis B or C

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