scholarly journals Relationships of body composition and liver fat content with insulin resistance in obesity-matched adolescents and adults

Obesity ◽  
2014 ◽  
Vol 22 (5) ◽  
pp. 1325-1331 ◽  
Author(s):  
Katarzyna Linder ◽  
Fabian Springer ◽  
Jürgen Machann ◽  
Fritz Schick ◽  
Andreas Fritsche ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Composition ◽  
Fat Content ◽  
Liver Fat ◽  
Liver Fat Content ◽  
Adolescents And Adults

scholarly journals Effects of Identical Weight Loss on Body Composition and Features of Insulin Resistance in Obese Women With High and Low Liver Fat Content

Diabetes ◽  
2003 ◽  
Vol 52 (3) ◽  
pp. 701-707 ◽  
Author(s):  
M. Tiikkainen ◽  
R. Bergholm ◽  
S. Vehkavaara ◽  
A. Rissanen ◽  
A.-M. Hakkinen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Body Composition ◽  
Fat Content ◽  
Liver Fat ◽  
Obese Women ◽  
Liver Fat Content

Liver steatosis coexists with myocardial insulin resistance and coronary dysfunction in patients with type 2 diabetes

2006 ◽  
Vol 291 (2) ◽  
pp. E282-E290 ◽  
Author(s):  
Riikka Lautamäki ◽  
Ronald Borra ◽  
Patricia Iozzo ◽  
Markku Komu ◽  
Terho Lehtimäki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Liver Steatosis ◽  
Fat Content ◽  
Liver Fat ◽  
Liver Fat Content ◽  
Artery Disease ◽  
Myocardial Insulin Resistance ◽  
High Liver

Nonalcoholic fatty liver (NAFL) is a common comorbidity in patients with type 2 diabetes and links to the risk of coronary syndromes. The aim was to determine the manifestations of metabolic syndrome in different organs in patients with liver steatosis. We studied 55 type 2 diabetic patients with coronary artery disease using positron emission tomography. Myocardial perfusion was measured with [15O]H2O and myocardial and skeletal muscle glucose uptake with 2-deoxy-2-[18F]fluoro-d-glucose during hyperinsulinemic euglycemia. Liver fat content was determined by magnetic resonance proton spectroscopy. Patients were divided on the basis of their median (8%) into two groups with low (4.6 ± 2.0%) and high (17.4 ± 8.0%) liver fat content. The groups were well matched for age, BMI, and fasting plasma glucose. In addition to insulin resistance at the whole body level ( P = 0.012) and muscle ( P = 0.002), the high liver fat group had lower insulin-stimulated myocardial glucose uptake ( P = 0.040) and glucose extraction rate ( P = 0.0006) compared with the low liver fat group. In multiple regression analysis, liver fat content was the most significant explanatory variable for myocardial insulin resistance. In addition, the high liver fat group had increased concentrations of high sensitivity C-reactive protein, soluble forms of E-selectin, vascular adhesion protein-1, and intercellular adhesion molecule-1 ( P < 0.05) and lower coronary flow reserve ( P = 0.02) compared with the low liver fat group. In conclusion, in patients with type 2 diabetes and coronary artery disease, liver fat content is a novel independent indicator of myocardial insulin resistance and reduced coronary functional capacity. Further studies will reveal the effect of hepatic fat reduction on myocardial metabolism and coronary function.

Effect of liver fat on insulin clearance

2007 ◽  
Vol 293 (6) ◽  
pp. E1709-E1715 ◽  
Author(s):  
Anna Kotronen ◽  
Satu Vehkavaara ◽  
Anneli Seppälä-Lindroos ◽  
Robert Bergholm ◽  
Hannele Yki-Järvinen
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Fat Content ◽  
Insulin Clearance ◽  
Liver Fat ◽  
Hepatic Insulin Resistance ◽  
Model Assessment ◽  
Liver Fat Content ◽  
Hepatic Insulin Sensitivity ◽  
Impaired Insulin

A fatty liver is associated with fasting hyperinsulinemia, which could reflect either impaired insulin clearance or hepatic insulin action. We determined the effect of liver fat on insulin clearance and hepatic insulin sensitivity in 80 nondiabetic subjects [age 43 ± 1 yr, body mass index (BMI) 26.3 ± 0.5 kg/m2]. Insulin clearance and hepatic insulin resistance were measured by the euglycemic hyperinsulinemic (insulin infusion rate 0.3 mU·kg−1·min−1for 240 min) clamp technique combined with the infusion of [3-3H]glucose and liver fat by proton magnetic resonance spectroscopy. During hyperinsulinemia, both serum insulin concentrations and increments above basal remained ∼40% higher ( P < 0.0001) in the high (15.0 ± 1.5%) compared with the low (1.8 ± 0.2%) liver fat group, independent of age, sex, and BMI. Insulin clearance (ml·kg fat free mass−1·min−1) was inversely related to liver fat content ( r = −0.52, P < 0.0001), independent of age, sex, and BMI ( r = −0.37, P = 0.001). The variation in insulin clearance due to that in liver fat (range 0–41%) explained on the average 27% of the variation in fasting serum (fS)-insulin concentrations. The contribution of impaired insulin clearance to fS-insulin concentrations increased as a function of liver fat. This implies that indirect indexes of insulin sensitivity, such as homeostatic model assessment, overestimate insulin resistance in subjects with high liver fat content. Liver fat content correlated significantly with fS-insulin concentrations adjusted for insulin clearance ( r = 0.43, P < 0.0001) and with directly measured hepatic insulin sensitivity ( r = −0.40, P = 0.0002). We conclude that increased liver fat is associated with both impaired insulin clearance and hepatic insulin resistance. Hepatic insulin sensitivity associates with liver fat content, independent of insulin clearance.

scholarly journals Effect of Weight Loss on Liver Free Fatty Acid Uptake and Hepatic Insulin Resistance

2009 ◽  
Vol 94 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Antti P. M. Viljanen ◽  
Patricia Iozzo ◽  
Ronald Borra ◽  
Mikko Kankaanpää ◽  
Anna Karmi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fatty Acid Uptake ◽  
Fat Content ◽  
Liver Fat ◽  
Hepatic Insulin Resistance ◽  
Acid Uptake ◽  
Liver Fat Content

Abstract Objective: Weight loss has been shown to decrease liver fat content and whole-body insulin resistance. The current study was conducted to investigate the simultaneous effects of rapid weight reduction with a very-low-calorie diet on liver glucose and fatty acid metabolism and liver adiposity. Hypothesis: We hypothesized that liver insulin resistance and free fatty acid uptake would decrease after weight loss and that they are associated with reduction of liver fat content. Design: Thirty-four healthy obese subjects (body mass index, 33.7 ± 8.0 kg/m2) were studied before and after a very-low-calorie diet for 6 wk. Hepatic glucose uptake and endogenous glucose production were measured with [18F]fluorodeoxyglucose during hyperinsulinemic euglycemia and fasting hepatic fatty acid uptake with [18F]fluoro-6-thia-heptadecanoic acid and positron emission tomography. Liver volume and fat content were measured using magnetic resonance imaging and spectroscopy. Results: Subjects lost weight (11.2 ± 2.9 kg; P &lt; 0.0001). Liver volume decreased by 11% (P &lt; 0.002), which was partly explained by decreased liver fat content (P &lt; 0.0001). Liver free fatty acid uptake was 26% lower after weight loss (P &lt; 0.003) and correlated with the decrement in liver fat content (r = 0.54; P &lt; 0.03). Hepatic glucose uptake during insulin stimulation was unchanged, but the endogenous glucose production decreased by 40% (P &lt; 0.04), and hepatic insulin resistance by 40% (P &lt; 0.05). Conclusions: The liver responds to a 6-wk period of calorie restriction with a parallel reduction in lipid uptake and storage, accompanied by enhancement of hepatic insulin sensitivity and clearance.

Mitochondrial diabetes is associated with insulin resistance in subcutaneous adipose tissue but not with increased liver fat content

2011 ◽  
Vol 34 (6) ◽  
pp. 1205-1212 ◽  
Author(s):  
Markus M. Lindroos ◽  
Ronald Borra ◽  
Nina Mononen ◽  
Terho Lehtimäki ◽  
Kirsi A. Virtanen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Fat Content ◽  
Liver Fat ◽  
Liver Fat Content ◽  
Mitochondrial Diabetes ◽  
Subcutaneous Adipose

scholarly journals Correlation between liver fat content with dyslipidemia and Insulin resistance

2013 ◽  
Vol 17 (7) ◽  
pp. 355 ◽  
Author(s):  
Sanjay Saran ◽  
Rajeev Philip ◽  
Manish Gutch ◽  
Rajeev Tyagi ◽  
Puspalata Agroiya ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fat Content ◽  
Liver Fat ◽  
Liver Fat Content

scholarly journals The liver–alpha cell axis associates with liver fat and insulin resistance: a validation study in women with non-steatotic liver fat levels

Diabetologia ◽  
2020 ◽  
Author(s):  
Christina Gar ◽  
Stefanie J. Haschka ◽  
Stefanie Kern-Matschilles ◽  
Barbara Rauch ◽  
Vanessa Sacco ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fat Content ◽  
Alpha Cell ◽  
Liver Fat ◽  
Regression Analyses ◽  
Liver Fat Content ◽  
Cell Axis ◽  
The Metabolic Syndrome

Abstract Aims/hypothesis Many individuals who develop type 2 diabetes also display increased glucagon levels (hyperglucagonaemia), which we have previously found to be associated with the metabolic syndrome. The concept of a liver–alpha cell axis provides a possible link between hyperglucagonaemia and elevated liver fat content, a typical finding in the metabolic syndrome. However, this association has only been studied in individuals with non-alcoholic fatty liver disease. Hence, we searched for a link between the liver and the alpha cells in individuals with non-steatotic levels of liver fat content. We hypothesised that the glucagon–alanine index, an indicator of the functional integrity of the liver–alpha cell axis, would associate with liver fat and insulin resistance in our cohort of women with low levels of liver fat. Methods We analysed data from 79 individuals participating in the Prediction, Prevention and Subclassification of Type 2 Diabetes (PPSDiab) study, a prospective observational study of young women at low to high risk for the development of type 2 diabetes. Liver fat content was determined by MRI. Insulin resistance was calculated as HOMA-IR. We conducted Spearman correlation analyses of liver fat content and HOMA-IR with the glucagon–alanine index (the product of fasting plasma levels of glucagon and alanine). The prediction of the glucagon–alanine index by liver fat or HOMA-IR was tested in multivariate linear regression analyses in the whole cohort as well as after stratification for liver fat content ≤0.5% (n = 39) or >0.5% (n = 40). Results The glucagon–alanine index significantly correlated with liver fat and HOMA-IR in the entire cohort (ρ = 0.484, p < 0.001 and ρ = 0.417, p < 0.001, respectively). These associations resulted from significant correlations in participants with a liver fat content >0.5% (liver fat, ρ = 0.550, p < 0.001; HOMA-IR, ρ = 0.429, p = 0.006). In linear regression analyses, the association of the glucagon–alanine index with liver fat remained significant after adjustment for age and HOMA-IR in all participants and in those with liver fat >0.5% (β = 0.246, p = 0.0.23 and β = 0.430, p = 0.007, respectively) but not in participants with liver fat ≤0.5% (β = −0.184, p = 0.286). Conclusions/interpretation We reproduced the previously reported association of liver fat content and HOMA-IR with the glucagon–alanine index in an independent study cohort of young women with low to high risk for type 2 diabetes. Furthermore, our data indicates an insulin-resistance-independent association of liver fat content with the glucagon–alanine index. In summary, our study supports the concept that even lower levels of liver fat (from 0.5%) are connected to relative hyperglucagonaemia, reflecting an imminent impairment of the liver–alpha cell axis.

ROLE OF ANDROGEN IN LIVER FAT CONTENT IN WOMEN: METABOLICALLY ADVANTAGEOUS OR DISADVANTAGEOUS?

2020 ◽  
Vol 26 (9) ◽  
pp. 1003-1016
Author(s):  
Yuying Wang ◽  
Xiaojing Guo ◽  
Wendi Xu ◽  
Jie Cai ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Fatty Liver Disease ◽  
Fat Content ◽  
Liver Fat ◽  
Glucose Regulation ◽  
Impaired Glucose Regulation ◽  
Liver Fat Content ◽  
Nonalcoholic Fatty Liver ◽  
Free Androgen Index

Objective: Androgens have a controversial effect on liver fat content (LFC) in androgen-excess females and androgen-deficient males. Polycystic ovarian syndrome (PCOS) is often associated with hyperandrogenism and nonalcoholic fatty liver disease. The aim of this study was to explore the association between hyperandrogenemia and increased liver fat content in women with PCOS, independent of other metabolic parameters. Methods: This case series study included 501 women with PCOS and 112 aged-matched controls in the outpatient department of a tertiary hospital. Anthropometric measurements, hepatic and renal function, glucose and lipid metabolism parameters, and sex hormones were examined in these women. LFC was measured by quantitative ultrasonography. Results: Women with hyperandrogenism ( P<.001), an oligomenorrhoea/anovulation phenotype ( P = .0064), and a diagnosis of PCOS ( P<.001) had higher LFC. Androgen level is an important factor among the 9 independent risk factors of LFC ( P = .0239) and may have a dimorphic impact on LFC. In all women, when the free androgen index (FAI) was less than 41.94, LFC increased with the elevated FAI; when the FAI was greater than 41.94, LFC decreased with the elevated FAI ( P<.001). In women with PCOS, receiver operating characteristic curve analysis demonstrated that LFC could at least partially predict impaired glucose regulation, impaired lipid metabolism, and insulin resistance ( P<.0001 for all). Conclusion: Androgen level is associated with LFC in dimorphic directions. LFC may be a predictive factor of insulin resistance, impaired glucose regulation, and impaired lipid metabolism in women with PCOS. Abbreviations: A2 = androstenedione; AUC = area under curve; BioT = bioactive testosterone; BMI = body mass index; DHEAS = sulfated dehydroepiandrosterone; FAI = free androgen index; FBG = fasting blood glucose; FFA = free fatty acid; FT = free testosterone; HA = hyperandrogenism; LFC = liver fat content; LH = luteinizing hormone; MRS = proton magnetic resonance; NAFLD = nonalcoholic fatty liver disease; ROC = receiver operator characteristic; SHBG = sex hormone binding globulin; T = total testosterone; T2DM = type 2 diabetes mellitus

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