Aminotransferase and gamma-glutamyl transpeptidase levels in obesity are associated with insulin resistance and the metabolic syndrome

Marchesini, Giulio; Avagnina, S; Barantani, E. G.; Ciccarone, Annamaria; Corica, Francesco; Dall’Aglio, Elisabetta; Grave, Riccardo Dalle; Morpurgo, Paola S.; Tomasi, Franco; Vitacolonna, Ester

doi:10.1007/bf03347199

Cited by 142 publications

(98 citation statements)

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“…A large Italian study of obese adults also showed elevated GGT to be associated with elevated triglycerides and hyperglycemia. [34]. In addition, a study of severely obese adults undergoing bariatric surgery showed a decrease in GGT to be the best predictor of improvement in inflammation, fibrosis, and non-alcoholic steatohepatitis (NASH).…”

Section: Discussionmentioning

confidence: 99%

Presence of the Metabolic Syndrome in Obese Adolescents Predicts Impaired Glucose Tolerance and Nonalcoholic Fatty Liver Disease

Love-Osborne

Nadeau²,

Sheeder

et al. 2008

Journal of Adolescent Health

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Purpose-To evaluate whether the presence of MS in obese adolescents is associated with other co-morbidities of obesity Methods-85 obese teens with fasting insulin > 25 uU/ml and family history of type 2 diabetes mellitus and/or acanthosis nigricans. Mean age 15.8 ± 1.7 years; body mass index 39.3 ± 6.6 kg/m2; 70% female; 54% Hispanic, 35% black. Laboratory analysis included fasting lipids, glucose, gamma gluteryl transferase (GGT), and oral glucose tolerance testing. Additional liver transaminases and liver ultrasound (US) were performed to evaluate presence and severity of fatty liver.Results-All subjects met MS criteria for children for waist circumference; 49% for blood pressure; 54% for high density lipoprotein (HDL); 54% for triglycerides; 20% for impaired fasting glucose or impaired glucose tolerance (IGT). 47 subjects had 3 or more MS criteria. BMI was no different between groups with and without MS. Subjects with 3 or more MS criteria were more likely to have IGT (p = .004), elevated ALT (p = .039), elevated GGT (p = .036), fatty liver on US (p < .001), and more severe fatty liver (p = .001).Reprint requests: kathryn.love-osborne@dhha.org, University of Colorado at Denver and Health Sciences Center, Denver Health and Hospitals Authority Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Conclusions-Abnormal glucose regulation and evidence of non-alcoholic fatty liver disease (NAFLD) were more common in subjects meeting 3 criteria for MS than in those meeting fewer criteria. The identification of MS provides value to the primary care provider. Those patients meeting criteria for MS should be evaluated for glucose intolerance and NAFLD. NIH Public Access

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Section: Discussionmentioning

confidence: 99%

Presence of the Metabolic Syndrome in Obese Adolescents Predicts Impaired Glucose Tolerance and Nonalcoholic Fatty Liver Disease

Love-Osborne

Nadeau²,

Sheeder

et al. 2008

Journal of Adolescent Health

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“…1 The number of patients at risk of advanced liver disease through nonalcoholic steatohepatitis (NASH) and cryptogenic cirrhosis is increasing because of the epidemics of obesity and diabetes related to western lifestyle, 2 associated with fatty liver 3,4 and raised alanine aminotransferase levels. [5][6][7] The pathogenesis of NAFLD is probably multifactorial, but insulin resistance, either genetically determined or obesity related, is a cornerstone. 8 A lot of experimental and clinical data point to NAFLD as the hepatic expression of the metabolic syndrome (MS).…”

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Endothelial dysfunction and cardiovascular risk profile in nonalcoholic fatty liver disease†

et al. 2005

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Nonalcoholic fatty liver disease (NAFLD) is consistently associated with features of the metabolic syndrome, a condition carrying a high risk of cardiovascular events. We measured the vasodilatory response of the brachial artery in response to ischemia (a test of endothelial function) (FMV) as well as cardiovascular risk profile in 52 NAFLD cases and 28 age-and sex-matched controls. The 10-year risk of coronary events was calculated according to the Framingham equation and the scores derived from the PROCAM study and NCEP-ATPIII proposals. FMV was 6.33% ؎ 5.93% in NAFLD versus 12.22% ؎ 5.05% in controls (P < .0001), and higher in pure fatty liver (9.93%) compared with nonalcoholic steatohepatitis (4.94%) (P ‫؍‬ .010). No differences were observed in flow-independent vasodilation (response to sublingual nitroglycerin). Percent FMV was negatively associated with insulin resistance (homeostasis model assessment) in the whole population (r ‫؍‬ ؊0.243; P ‫؍‬ .030). In logistic regression analysis, NAFLD was associated with a percent FMV in the lower tertile (OR, 6.7; 95% CI, 1.26-36.1), after adjustment for age, sex, body mass index, and insulin resistance. Among NAFLD patients, low FMV was associated with nonalcoholic steatohepatitis (adjusted OR, 6.8; 95% CI, 1.2-40.2). The 10-year probability of cardiovascular events was moderately increased in NAFLD, and particularly in nonalcoholic steatohepatitis. In conclusion, our study provides evidence of endothelial dysfunction and increased risk of cardiovascular events in NAFLD. The risk of advanced liver disease is well recognized in NAFLD patients, but the large majority of cases might experience cardiovascular disease in the long term, indirectly limiting the burden of liver failure. (HEPATOLOGY 2005;42:473-480.)

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“…In our opinion, gender differences in steatosis might also mirror derangements of other endocrine hormones, notably insulin, growth and thyroid hormones and cytokines, particularly adiponectin and leptin in NAFLD patients. 3 As far as GGT is concerned, this enzyme might be a simple and reliable marker of insulin resistance both in obesity 9 and in patients with NAFLD or HCV-related steatosis. 10 It is well known that both alanine aminotransferase and, more closely, GGT predict the onset of type 2 diabetes in the general population.…”

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confidence: 99%

Gender, fatty liver and GGT

et al. 2006

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We would like to comment on the paper by Cammà et al., 1 who report on gender differences in hepatitis C virus (HCV)-related steatosis and on elevated gamma-glutamyl transferase (GGT) values as a predictor of poor response to antiviral treatment. 1 In our opinion, these data could be better understood taking into account that HCV genotype 1-related steatosis closely resembles non-alcoholic fatty liver disease (NAFLD). 2 Interestingly, in unselected consecutive subjects referred by General Practitioners for the evaluation of a "bright" liver at ultrasound scanning and enrolled in the POLISTENA study, NAFLD also displays a gender-dimorphic pattern. Indeed, in the majority of studies published in the 2000-2005 literature, 3 it occurs more frequently in the male gender. 4 It is amazing that our results, which were collected in a series recruited in the GPs offices in Modena, 4 closely mirror those by Marchesini et al. in Bologna and Turin,5 in the context of metabolic and liver Units (Table 1). These data indicate that male patients with NAFLD are approximately 10 years younger than women with this condition. Women, though, tend to have a higher prevalence of metabolic derangements evaluated according to Adult Treatment Panel III.It is tempting to speculate that the circulating levels of estrogens within a physiological range might be responsible for a "protective" effect on the development of steatosis (due to both NAFLD and, presumably, HCV genotype 1). This would imply that women in the fertile age are relatively spared from the development of steatosis and that this protection vanes after menopause similar to what happens for cardiovascular disease. These findings are also supported by the association of NAFLD with the use of the anti-estrogen tamoxifen, 6 by the better profile of liver function enzymes in post-menopausal women taking hormone replacement therapy, 7 and finally by the finding that estradiol improves insulin sensitivity, 8 possibly preventing or reducing fat accumulation. In our opinion, gender differences in steatosis might also mirror derangements of other endocrine hormones, notably insulin, growth and thyroid hormones and cytokines, particularly adiponectin and leptin in NAFLD patients. 3 As far as GGT is concerned, this enzyme might be a simple and reliable marker of insulin resistance both in obesity 9 and in patients with NAFLD or HCV-related steatosis. 10 It is well known that both alanine aminotransferase and, more closely, GGT predict the onset of type 2 diabetes in the general population. 10 These observations fit with the finding that insulin resistance impairs the response to antiviral treatment, 1 and lead us to conclude that elevated GGT, insulin resistance, and impaired response to antiviral treatment form an ominous triangle in the context of chronic HCV infection.In conclusion, advances in the pathogenesis of NAFLD made over the past few years might give new clues to the understanding and, possibly, the treatment of HCV-associated steatosis. 2

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Aminotransferase and gamma-glutamyl transpeptidase levels in obesity are associated with insulin resistance and the metabolic syndrome

Cited by 142 publications

References 38 publications

Presence of the Metabolic Syndrome in Obese Adolescents Predicts Impaired Glucose Tolerance and Nonalcoholic Fatty Liver Disease

Presence of the Metabolic Syndrome in Obese Adolescents Predicts Impaired Glucose Tolerance and Nonalcoholic Fatty Liver Disease

Endothelial dysfunction and cardiovascular risk profile in nonalcoholic fatty liver disease†

Gender, fatty liver and GGT

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