Rosiglitazone Inhibits Hepatic Insulin Resistance Induced by Chronic Pancreatitis and IKK-β/NF-κB Expression in Liver

Zhou, Xiaolei; You, Shengyi

doi:10.1097/mpa.0000000000000173

Cited by 27 publications

(19 citation statements)

References 37 publications

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“…Our study implies an increment in dimethylarginines caused by rosiglitazone treatment in acute liver injury. Our findings also indicate an antioxidant activity of rosiglitazone in the liver tissue, being in good agreement with other reports [34,35]. To our knowledge, this is first study with respect to the effect of rosiglitazone on the activity of DDAH.…”

Section: Discussionsupporting

confidence: 95%

Effect of rosiglitazone on asymmetric dimethylarginine metabolism in thioacetamide-induced acute liver injury

et al. 2015

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Section: Discussionsupporting

confidence: 95%

Effect of rosiglitazone on asymmetric dimethylarginine metabolism in thioacetamide-induced acute liver injury

et al. 2015

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“…Rosiglitazone has been shown to reverse hepatic insulin resistance in rats with chronic pancreatitis, but has not been rigorously studied in human beings. 45 …”

Section: Diabetes Secondary To Chronic Pancreatitismentioning

confidence: 99%

Type 3c (pancreatogenic) diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer

Hart

Bellin

Andersen

et al. 2016

The Lancet Gastroenterology & Hepatology

385

319

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Diabetes mellitus is a group of diseases defined by persistent hyperglycaemia. Type 2 diabetes, the most prevalent form, is characterised initially by impaired insulin sensitivity and subsequently by an inadequate compensatory insulin response. Diabetes can also develop as a direct consequence of other diseases, including diseases of the exocrine pancreas. Historically, diabetes due to diseases of the exocrine pancreas was described as pancreatogenic or pancreatogenous diabetes mellitus, but recent literature refers to it as type 3c diabetes. It is important to note that type 3c diabetes is not a single entity; it occurs because of a variety of exocrine pancreatic diseases with varying mechanisms of hyperglycaemia. The most commonly identified causes of type 3c diabetes are chronic pancreatitis, pancreatic ductal adenocarcinoma, haemochromatosis, cystic fibrosis, and previous pancreatic surgery. In this Review, we discuss the epidemiology, pathogenesis, and clinical relevance of type 3c diabetes secondary to chronic pancreatitis and pancreatic ductal adenocarcinoma, and highlight several important knowledge gaps.

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“…Pancreatic exocrine insufficiency (PEI) results in maldigestion of fat and other nutrients thereby culminating in malnutrition and metabolic abnormalities. DM secondary to CP is distinct from Type I and Type II DM; and is characterised by insulin deficiency coupled with absence of glucagon and pancreatic polypeptide regulatory responses, and hepatic insulin resistance234. Even though oral microbial dysbiosis and small intestinal bacterial overgrowth (SIBO) has been reported in patients with CP56, the detailed alterations in the taxa of the intestinal microbiota in this illness has not been studied.…”

mentioning

confidence: 99%

Altered intestinal microbiota in patients with chronic pancreatitis: implications in diabetes and metabolic abnormalities

Jandhyala

Madhulika

Deepika

et al. 2017

Sci Rep

111

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Intestinal dysbiosis and its functional implications in chronic pancreatitis (CP) have not been elaborately studied. We evaluated the taxonomic and functional alterations in intestinal microbiota in 30 well-characterised patients with CP (16 without, 14 with diabetes) and 10 healthy controls. The patients with CP and diabetes had significantly longer disease duration and greater degree of malnutrition. There was increase in plasma endotoxin concentrations from controls to CP non-diabetics to CP diabetics. We observed significant differences in richness and alpha diversity between the groups. We also observed increase in the Firmicutes:Bacteroidetes ratio in CP patients without and with diabetes. There was reduction in abundance of Faecalibacterium prausnitzii and Ruminococcus bromii from controls to CP non-diabetics to CP diabetics. On the other hand, there was increase in LPS (endotoxin) synthetic pathways (KEGG orthology) in the groups. Faecalibacterium prausnitzii abundance correlated negatively with plasma endotoxin and glycemic status; while plasma endotoxin correlated positively with blood glucose and negatively with plasma insulin. Our results have important implications for future studies exploring mechanistic insights on secondary diabetes in CP.

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Rosiglitazone Inhibits Hepatic Insulin Resistance Induced by Chronic Pancreatitis and IKK-β/NF-κB Expression in Liver

Abstract: Rosiglitazone attenuates hepatic insulin resistance induced by CP. The inhibition of hepatic IKK-β and NF-κB expressions via peroxisome proliferator-activated receptor-γ may be involved in the therapeutic effect of rosiglitazone.

Cited by 27 publications

References 37 publications

Effect of rosiglitazone on asymmetric dimethylarginine metabolism in thioacetamide-induced acute liver injury

Effect of rosiglitazone on asymmetric dimethylarginine metabolism in thioacetamide-induced acute liver injury

Type 3c (pancreatogenic) diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer

Altered intestinal microbiota in patients with chronic pancreatitis: implications in diabetes and metabolic abnormalities

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