Chronic Liver Disease Among Two American Indian Patient Populations in the Southwestern United States, 2000-2003

Bialek, Stephanie R.; Redd, John T.; Lynch, Audrey; Vogt, Tara M.; Lewis, Sharon K.; Wilson, Charlton; Bell, Beth P.

doi:10.1097/mcg.0b013e318054492a

Cited by 30 publications

(27 citation statements)

References 14 publications

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“…Compared with non-Hispanic whites, Hispanic individuals have signifi cantly higher and nonHispanic blacks have signifi cantly lower prevalence of NAFLD ( 15,33 -35 ). Th e prevalence of NAFLD in American-Indian and The Diagnosis and Management of NAFLD Alaskan-Native populations appears lower, ranging from 0.6 to 2.2 % , although the lack of histologic defi nition makes it likely that is an underestimate ( 36,37 ). Th ere are data to suggest that hypothyroidism, hypopituitarism, hypogonadism, sleep apnea, and polycystic ovary syndrome independent of obesity are important risk factors for the presence of NAFLD ( Table 4 ) …”

Section: Prevalence Of Nafld In High-risk Groups ( Table 4 )mentioning

confidence: 98%

The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

Chalasani

Younossi

Lavine

et al. 2012

American Journal of Gastroenterology

355

222

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Section: Prevalence Of Nafld In High-risk Groups ( Table 4 )mentioning

confidence: 98%

The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

Chalasani

Younossi

Lavine

et al. 2012

American Journal of Gastroenterology

355

222

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“…15,[33][34][35] The prevalence of NAFLD in American-Indian and Alaskan-Native populations appears lower, ranging from 0.6% to 2.2%, although the lack of histologic definition makes it likely that is an underestimate. 36,37 There are data to suggest that hypothyroidism, hypopituitarism, hypogonadism, sleep apnea, and polycystic ovary syndrome independent of obesity are important risk factors for the presence of NAFLD (Table 4). 3 …”

Section: Strength Of Recommendationmentioning

confidence: 99%

The diagnosis and management of non-alcoholic fatty liver disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

et al. 2012

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“…The mechanism for this protective effect may relate to the fact that emodin efficiently inhibits HSC activation in vivo. Hepatic fibrosis, which may lead to cirrhosis, is associated with most chronic liver diseases [22] . Hepatic fibrosis is thought to be a reversible disease, however, there is no satisfactory method in clinical practice to reverse the pathological process yet [23] .…”

Section: Discussionmentioning

confidence: 99%

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Dong¹,

Yan²,

Zhang³

et al. 2009

WJG

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AIM: To investigate the role of emodin in protecting the liver against fibrogenesis caused by carbon tetrachloride (CCl4) in rats and to further explore the underlying mechanisms. METHODS:Rat models of experimental hepatic fibrosis were established by injection with CCl4; the treated rats received emodin via oral administration at a dosage of 20 mg/kg twice a week at the same time. Rats injected with olive oil served as a normal group. Histopathological changes were observed by hematoxylin and eosin staining. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and hepatic hydroxyproline content were assayed by biochemical analyses. The mRNA and protein relevant to hepatic stellate cell (HSC) activation in the liver were assessed using real-time reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, western blotting and enzymelinked immunosorbent assay. RESULTS:The degree of hepatic fibrosis increased markedly in the CCl4 group compared to the normal group (P < 0.01), and decreased markedly in the emodin group compared to the CCl4 group according to METAVIR scale (P < 0.01) compared with those in the normal control group (51.02 ± 10.64 IU/L and 132.28 ± 18.14 IU/L). The activities of serum ALT and AST were significantly higher in rats injected with CCl4 (289.25 ± 68.84 IU/L and 423.89 ± 35.67 IU/L, both P < 0.05).The activities of serum ALT and AST were significantly reduced by administration of emodin (176.34 ± 4 7. 2 9 I U / L a n d 2 2 6 . 1 ± 4 4. 5 2 I U / L , b o t h P < 0.05). Compared with the normal controls (54.53 ± 13.46 mg/g), hepatic hydroxyproline content was significantly higher in rats injected with CCl4 (120.27 ± 28.47 mg/g, P < 0.05). Hepatic hydroxyproline content was significantly reduced in the rats treated with emodin at 20 mg/kg (71.25 ± 17.02 mg/g, P < 0.05).Emodin significantly protected the liver from injury by reducing serum AST and ALT activities and reducing hepatic hydroxyproline content. The mRNA levels of transforming growth factor-β1 (TGF-β1), Smad4 and α-SMA in liver tissues were significantly down-regulated in SD rats that received emodin treatment. Furthermore, significant down-regulation of serum TGF-β1 protein levels and protein expression of Smad4 and α-SMA in liver tissues was also observed in the rats. Emodin inhibited HSC activation by reducing the abundance of TGF-β1 and Smad4. CONCLUSION:Emodin protects the rat liver from CCl4-induced fibrogenesis by inhibiting HSC activation. Emodin might be a therapeutic antifibrotic agent for the treatment of hepatic fibrosis.

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Chronic Liver Disease Among Two American Indian Patient Populations in the Southwestern United States, 2000-2003

Cited by 30 publications

References 14 publications

The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

The diagnosis and management of non-alcoholic fatty liver disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

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Chronic Liver Disease Among Two American Indian Patient Populations in the Southwestern United States, 2000-2003

Cited by 30 publications

References 14 publications

The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

The diagnosis and management of non-alcoholic fatty liver disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

Emodin protects rat liver from CCl4-induced fibrogenesis via inhibition of hepatic stellate cells activation

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Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation