Contribution of β-cell dysfunction and insulin resistance to cirrhosis-associated diabetes: Role of severity of liver disease

Grancini, Valeria; Trombetta, Maddalena; Lunati, Maria Elena; Zimbalatti, Dario; Boselli, Maria Linda; Gatti, Stefano; Donato, Maria Francesca; Resi, Veronica; D’Ambrosio, Roberta; Aghemo, Alessio; Pugliese, Giuseppe; Bonadonna, Riccardo C.; Orsi, Emanuela

doi:10.1016/j.jhep.2015.08.011

Cited by 66 publications

(87 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…; 86.7% and 55.4% in this study by Jeon et al . and 88.3% and 59.6% in this study by Grancini et al . In contrast, in the cohort described by Marselli et al., 59% of subjects had NGT, whereas only 41% had abnormal glucose regulation (16% with IFG and/or IGT and 35% with DM).…”

Section: Epidemiologycontrasting

confidence: 45%

“…showed a DM incidence of 35.3% after a 4‐year follow‐up in patients with deteriorating liver function vs 21.2% in the whole cohort. More recently, we reported that DM was present in 20.5% of Child‐Pugh Class A, 56.1% of Child‐Pugh Class B, and 61.2% of Child‐Pugh Class C patients, whereas Marselli et al . did not find significant differences in the prevalence of DM or pre‐DM across Child‐Pugh classes.…”

Section: Epidemiologymentioning

confidence: 63%

“…of 34.4%. In addition, three studies in cirrhotic patients on the waiting list for OLT (including two surveys from our group) reported prevalence values of 41.7%, 27.2%, and 30.7%, respectively, for overt DM, and 16.6%, 3.4%, and 10.3%, respectively, for IFG.…”

Section: Epidemiologymentioning

confidence: 80%

“…In addition to these mechanisms, which may be operating before the development of cirrhosis in relation to specific aetiologies, liver decompensation seems to impair insulin secretion directly. A recent report from our group has provided important insights into the relative contribution of β‐cell dysfunction and insulin resistance to hepatogenous diabetes by analysing the results of an extended OGTT in a large cohort of cirrhotic patients . Results showed a significant and comparable reduction in insulin sensitivity in IGT and DM vs NGT patients, whereas β‐cell function was significantly impaired in DM, but not (or to a lesser extent) in IGT individuals.…”

Section: Pathophysiologymentioning

confidence: 99%

See 3 more Smart Citations

Hepatogenous diabetes: Is it time to separate it from type 2 diabetes?

Orsi

Grancini

Menini

et al. 2016

Liver International

Self Cite

View full text Add to dashboard Cite

By definition, hepatogenous diabetes is directly caused by loss of liver function, implying that it develops after cirrhosis onset. Therefore, it should be distinguished from type 2 diabetes developing before cirrhosis onset, in which specific causes of liver disease play a major role, in addition to traditional risk factors. Currently, although hepatogenous diabetes shows distinct pathophysiological and clinical features, it is not considered as an autonomous entity. Recent evidence suggests that the failing liver exerts an independent "toxic" effect on pancreatic islets resulting in β-cell dysfunction. Moreover, patients with hepatogenous diabetes usually present with normal fasting glucose and haemoglobin A levels and abnormal response to an oral glucose tolerance test, which is therefore required for diagnosis. This article discusses the need to separate hepatogenous diabetes from type 2 diabetes occurring in subjects with chronic liver disease and to identify individuals suffering from this condition for prognostic and therapeutic purposes.

show abstract

Section: Epidemiologycontrasting

confidence: 45%

Section: Epidemiologymentioning

confidence: 63%

Section: Epidemiologymentioning

confidence: 80%

Section: Pathophysiologymentioning

confidence: 99%

See 2 more Smart Citations

Hepatogenous diabetes: Is it time to separate it from type 2 diabetes?

Orsi

Grancini

Menini

et al. 2016

Liver International

Self Cite

View full text Add to dashboard Cite

show abstract

“…Az úgynevezett hepatogen diabetesben magasabb a széruminzulinszint, mint a klasszikus, 2-es típusú DM-ben. Ez a jelenség valószínűleg a portoszisztémás söntök és a kóros májmű-ködés által okozott csökkent májbéli kiválasztás (inzulinclearance↓) miatt alakul ki [20].…”

Section: Inzulinrezisztenciaunclassified

Az idült májbetegségek progressziójához vezető folyamatok

et al. 2016

View full text Add to dashboard Cite

Különböző károsító hatások miatt (vírusok, anyagcserezavarok, táplálkozási tényezők, toxikus ártalmak, autoimmun folyamatok) kóros májműködés lép fel, amely a máj elzsírosodásához és kötőszövetes átépüléséhez vezet. A progreszszió folyamata összetett, több útvonalon megy végbe, számos tényező befolyásolja. A szerzők összefoglaló közlemé-nyükben áttekintik a krónikus májbetegségek progressziójában részt vevő tényezőket. Bemutatják a sejtek szerepét, az általuk termelt főbb citokineket és gyulladásos mediátorokat, valamint az intestinalis bélflóra kapcsolatát a betegséggel. Kitérnek az oxidatív stressz, a mitokondriális diszfunkció és a sejthalál kórlefolyásban betöltött szerepére. Ismertetik az inzulinrezisztencia és a mikroelemek (vas, réz) kapcsolatát a májkárosodással. Összefoglalják a progreszszió hátterében álló genetikai és epigenetikai vonatkozásokat is. Az új kezelési lehetőségek felismerése, a kezelés hatékonyságának megítélése vagy a májátültetés időpontjának megválasztása, sikeressége függhet a kórlefolyás pontosabb megismerésétől. Orv. Hetil., 2016, 157(8), 290-297.Kulcsszavak: májelzsírosodás, progresszió, hepatitis, fibrosis, oxidatív stressz, mitokondriális diszfunkció, csillagsejtek, intestinalis bélflóra Various pathways leading to the progression of chronic liver diseasesAs the result of various effects (viruses, metabolic diseases, nutritional factors, toxic agents, autoimmune processes) abnormal liver function, liver steatosis and connective tissue remodeling may develop. Progression of this process is complex including various pathways and a number of factors. The authors summarize the factors involved in the progression of chronic liver disease. They describe the role of cells and the produced inflammatory mediators and cytokines, as well as the relationship between the disease and the intestinal flora. They emphasize the role of oxidative stress, mitochondrial dysfunction and cell death in disease progression. Insulin resistance and micro-elements (iron, copper) in relation to liver damage are also discussed, and genetic and epigenetic aspects underlying disease progression are summarized. Discovery of novel treatment options, assessment of the effectiveness of treatment, as well as the success and proper timing of liver transplantation may depend on a better understanding of the process of disease progression.Keywords: liver steatosis, progression, hepatitis, fibrosis, oxidative stress, mitochondrial dysfunction, stellate cells, intestinal flora Egresi, A., Lengyel, G., Somogyi, A., Blázovics, A., Hagymási, K. [Various pathways leading to the progression of chronic liver diseases]. Orv. Hetil., 2016, 157(8), 290-297. (Beérkezett: 2015 elfogadva: 2016. január Rövidítések AFLD = alkoholos zsírmájbetegség; ATP = adenozin-5'-trifoszfát; CCR5 = kemokinligand-5; CRP = C-reaktív protein; Cu = réz; DM = diabetes mellitus; DNS = deoxiribonukleinsav; ECM = extracelluláris mátrix; ETC = elektrontranszportlánc; FXR = farnezoid X-receptor; HBV = hepatitis B-vírus; HCV = hepatitis C-vírus; HSC = (h...

show abstract

Poor glycemic control in type‐2 diabetic patients infected with hepatitis B: A retrospective propensity‐matched study

Cai

Yue

et al. 2023

Journal of Medical Virology

View full text Add to dashboard Cite

Hepatitis B virus (HBV) infection and type-2 diabetes mellitus (T2DM) affect millions of individuals worldwide, whereas their interplay remains largely unclear. Here, we analyzed a large cohort of 330 HBV-infected inpatients with T2DM (so-called HBV + T2DM patients) and 330 T2DM inpatients without HBV infection (T2DM patients). Poor glycemic control was defined by glycated hemoglobin (HbA1c) ≥ 7%.Among 330 HBV + T2DM patients, 252 (76%) aged ≥ 50 years, 223 (68%) were males, 205 (62%) experienced poor glycemic control. The propensity-score matching approach was applied to match patient age, gender, comorbidities, and antidiabetic treatment between T2DM + HBV and T2DM patients. Compared with T2DM patients, HBV + T2DM patients had poorer glycemic control, longer hospitalization length, and higher alanine aminotransferase (p < 0.05). HBV + T2DM patients with HBV DNA ≥ 100 IU/mL or HBsAg ≥ 0.05 IU/mL had worse HbA1c control than T2DM patients without HBV infection (p < 0.05). HBV + T2DM patients who received no anti-HBV therapy had worse HbA1c control than HBV + T2DM patients receiving anti-HBV therapy (p < 0.05). Both insulin and anti-HBV therapy were significant factors associated with glycemic control in HBV + T2DM patients.Overall, HBV + T2DM patients exhibited poorer glycemic control than T2DM patients, but their clinical outcomes were likely improved by insulin plus anti-HBV treatment. Early management of HBV infection likely contributes to better clinical outcomes in HBV-infected patients with T2DM.

show abstract

Contribution of β-cell dysfunction and insulin resistance to cirrhosis-associated diabetes: Role of severity of liver disease

Cited by 66 publications

References 31 publications

Hepatogenous diabetes: Is it time to separate it from type 2 diabetes?

Hepatogenous diabetes: Is it time to separate it from type 2 diabetes?

Az idült májbetegségek progressziójához vezető folyamatok

Poor glycemic control in type‐2 diabetic patients infected with hepatitis B: A retrospective propensity‐matched study

Contact Info

Product

Resources

About