Insulin Resistance in Obesity: Metabolic Mechanisms and Measurement Methods

Belfiore, Francesco; Iannello, Silvia

doi:10.1006/mgme.1998.2727

Cited by 67 publications

(37 citation statements)

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“…[8][9][10][11] Several clinical factors (e.g., the presence of insulin-resistance syndrome) may promote these events, but other potentially important factors (e.g., predisposing genes and environmental factors) remain undefined. 4,13,14,16,[35][36][37][38][39] This study examined differential gene and protein expression profiles of patients within the NAFLD spectrum for whom extensive clinical and histological data were available. This approach has led to the development of a database integrating gene expression, protein expression, and clinical and biochemical data for a large cohort of patients with biopsy-proven NAFLD.…”

Section: Discussionmentioning

confidence: 99%

“…2,4,5 Both endogenous and exogenous factors may influence differential progression of these liver diseases. [11][12][13][14][15][16] For example, environmental factors contributing to oxidative stress may compound hepatic injury in some patients, whereas genetic factors may be more important in others. [17][18][19][20][21] Furthermore, an interaction among these factors may influence the disease course and tip the balance in favor of progression.…”

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confidence: 99%

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A genomic and proteomic study of the spectrum of nonalcoholic fatty liver disease

et al. 2005

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Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and some of its forms are progressive. This study describes the profiling of hepatic gene expression and serum protein content in patients with different subtypes of NAFLD. Liver biopsy specimens from 98 bariatric surgery patients were classified as normal, steatosis alone, steatosis with nonspecific inflammation, and nonalcoholic steatohepatitis (NASH). Microarray hybridizations were performed in triplicate and the microarray expression levels of a selected group of genes were confirmed using real-time quantitative reverse-transcriptase polymerase chain reaction. Serum protein profiles of the same patients were determined by SELDI-TOF mass spectrometry. Of 98 obese patients, 91 were diagnosed with NAFLD (12 steatosis alone, 52 steatosis with nonspecific inflammation, and 27 NASH), and 7 patients without NAFLD served as obese controls. Each group of NAFLD patients was compared with the obese controls, and 22 genes with more than twofold differences in expression levels were revealed. Proteomics analyses were performed for the same group comparisons and revealed twelve significantly different protein peaks. In conclusion, this genomic/proteomic analysis suggests differential expression of several genes and protein peaks in patients within and across the forms of NAFLD. These findings may help clarify the pathogenesis of NAFLD and identify potential targets for therapeutic intervention. (HEPATOLOGY 2005;42:665-674.)

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Section: Discussionmentioning

confidence: 99%

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A genomic and proteomic study of the spectrum of nonalcoholic fatty liver disease

et al. 2005

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“…[30][31][32] An abnormality in one liver function test is seen in up to 57% of unselected outpatients with diabetes. 33 Among male diabetics, the risk of NAFLD and hepatocellular carcinoma is double that of non-diabetics.…”

Section: Hypertension Metabolic Syndrome and Fatty Livermentioning

confidence: 99%

Hypertension and fatty liver: guilty by association?

Brookes

Cooper

2007

J Hum Hypertens

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“…For example, insulin resistance will result in increased free fatty acids while free fatty acids increase insulin resistance. 99 Regardless of mechanisms, abnormalities that are components of the metabolic syndrome are associated with and likely predispose to PE. 100 Pre-pregnancy obesity has a dose response relationship to PE.…”

Section: Maternal-fetal Interactions: Insulin Resistance and The Matementioning

confidence: 99%

Hypertension in pregnancy

Pipkin

Roberts

2000

J Hum Hypertens

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Hypertension arising during pregnancy remains one of the two most frequently-cited causes of maternal death in the UK. In some cases, pregnancy is unmasking underlying hypertension, which manifests itself in later life. Pregnant women who develop de novo proteinuric hypertension (pre-eclampsia, PE) can share many risk factors with patients with the metabolic syndrome, such as obesity, dyslipidaemia and insulin resistance. However, more than half the women who develop PE remain normotensive thereafter. There is a genetic component(s) to the disease, but it is most improbable that there is a 'PE gene'. Rather, there are factors such as geneticallydetermined thrombophilias which are predisposers but not prerequisites. Impaired placentation is a feature, with inadequate invasion of the spiral arteries by syncytiotrophoblast and poor remodelling. However, similiar features are found in association with non-hypertensive

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Insulin Resistance in Obesity: Metabolic Mechanisms and Measurement Methods

Cited by 67 publications

References 0 publications

A genomic and proteomic study of the spectrum of nonalcoholic fatty liver disease

A genomic and proteomic study of the spectrum of nonalcoholic fatty liver disease

Hypertension and fatty liver: guilty by association?

Hypertension in pregnancy

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