Eradication of insulin resistance

Imai, Junta; Yamada, Tetsuya; Saitō, Tsunemasa; Ishigaki, Yasushi; Hinokio, Yoshinori; Kotake, Hidetoshi; Oka, Yoshitomo; Katagiri, Hideki

doi:10.1016/s0140-6736(09)60872-2

Cited by 31 publications

(24 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This study supports a previous study in which similar outcomes were obtained [2] and a recent case report showing the long-term cure of IR by H. pylori eradication [3].…”

supporting

confidence: 92%

Helicobacter Pylori and Insulin Resistance: Time to Do Interventional Studies

Pellicano

Rizzetto

2009

Dig Dis Sci

View full text Add to dashboard Cite

“…This study supports a previous study in which similar outcomes were obtained [2] and a recent case report showing the long-term cure of IR by H. pylori eradication [3].…”

supporting

confidence: 92%

Helicobacter Pylori and Insulin Resistance: Time to Do Interventional Studies

Pellicano

Rizzetto

2009

Dig Dis Sci

View full text Add to dashboard Cite

“…11,12 Recently, an interesting case report showed that H. pylori eradication therapy ameliorated type B insulin resistance syndrome, for which there is no established effective therapy. 13 Reportedly, H. pylori infection occurs with a high frequency in patients with cirrhosis and hepatocellular carcinoma (HCC), which may explain the frequent occurrence of gastroduodenal ulcer in cirrhotic patients. [14][15][16][17] Several studies have shown that H. pylori genomic sequences could be detected in the liver of patients with HCC.…”

mentioning

confidence: 99%

Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

Goo

Park

et al. 2010

Laboratory Investigation

View full text Add to dashboard Cite

Our earlier report has shown that Helicobacter pylori promoted hepatic fibrosis in a murine model. Herein, in order to elucidate the mechanism by which H. pylori accelerate liver fibrosis, the authors investigated the changes in expression levels of mitogen-activated protein kinases (MAPKs), p53-related proteins, antioxidants, and proinflammatory cytokines in liver samples. H. pylori infection enhanced CCl 4 -induced MAP kinase activation and p53 signaling pathway as well as Bax-and proliferating-cell nuclear antigen expressions, whereas H. pylori alone induced neither of these expressions nor hepatic fibrosis. Moreover, mRNA expressions of inflammatory cytokines, glutathione peroxidase expression, and the proliferative index were strongly augmented in livers of the H. pylori with CCl 4 treatment group compared with those of the CCl 4 -alone treatment group, whereas there was no difference in apoptotic index between the two groups. Interestingly, H. pylori treatment increased the number of a-fetoprotein-expressing hepatocytes independently of CCl 4 intoxication. In vitro analyses, using an immortalized rat hepatic stellate cell (HSC) line, revealed that H. pylori lysates increased the proliferation of HSCs, which was boosted by the addition of transforming growth factor-beta1 (TGF-b1). Furthermore, the treatment of H. pylori lysates promoted the translocation of nuclear factor kappa-light-chain enhancer of activated B cells (NF-kB) into the nucleus based on an increase in the degradation of NF-kB inhibitor alpha, in the presence of TGF-b1, as did H 2 O 2 treatment. In conclusion, H. pylori infection along with an elevated TGF-b1 may accelerate hepatic fibrosis through increased TGF-b1-induced pro-inflammatory signaling pathways in HSCs. Moreover, H. pylori infection might increase the risk of TGF-b1-mediated tumorigenesis by disturbing the balance between apoptosis and proliferation of hepatocytes.

show abstract

“…We did not measure for the presence of the CagA protein and could not assess this hypothesis. Although the overall prevalence of H. pylori in the US is declining, seroprevalence is overall still high, especially in populations (older, minorities, overweight) who are at greatest risk for diabetes 35–37 and there is evidence that obesity may modify the association between H. pylori and glucose tolerance 18 . However, subgroup analyses by race/ethnicity and weight status did not reveal any significant associations.…”

Section: Discussionmentioning

confidence: 99%

H. pylori seroprevalence and risk of diabetes: An ancillary case–control study nested in the diabetes prevention program

Alzahrani

Nelson

Moss

et al. 2017

Journal of Diabetes and its Complications

View full text Add to dashboard Cite

OBJECTIVE To determine the association between H. pylori infection and risk of incident diabetes in adults at high risk for diabetes who participated in the Diabetes Prevention Program (DPP) study. METHODS In a nested case-control study conducted among 421 adults with newly diagnosed diabetes and 421 matched controls, we examined the association between serological status of H. pylori at baseline and risk of incident diabetes over a mean follow-up period of 2.6 years. Using data from the baseline visit of the DPP, we also examined the cross-sectional association between presence of H. pylori antibodies and insulin sensitivity, insulin secretion and the disposition index-like measure after a 75-gram oral glucose tolerance test (OGTT). RESULTS At baseline, H. pylori antibodies were present in 40% of participants who developed diabetes and 39% of controls. After adjusting for matching factors, there was no association between exposure to H. pylori and incident diabetes (odds ratio [OR] of 1.04 (95% CI, 0.77 to 1.40). In cross-sectional analyses, H. pylori status was not significantly associated with insulin sensitivity and disposition index-like measure from OGTT. CONCLUSIONS In adults at high risk for diabetes, H. pylori seropositivity was not associated with risk of developing diabetes.

show abstract

Eradication of insulin resistance

Cited by 31 publications

References 3 publications

Helicobacter Pylori and Insulin Resistance: Time to Do Interventional Studies

Helicobacter Pylori and Insulin Resistance: Time to Do Interventional Studies

Helicobacter pylori accelerates hepatic fibrosis by sensitizing transforming growth factor-β1-induced inflammatory signaling

H. pylori seroprevalence and risk of diabetes: An ancillary case–control study nested in the diabetes prevention program

Contact Info

Product

Resources

About