A diet low in sugar reduces the production of atherogenic lipoproteins in men with high liver fat

2015 ◽  
Vol 241 (1) ◽  
pp. e46 ◽  
Author(s):  
M. Umpleby ◽  
F. Shojaee-Moradie ◽  
B. Fielding ◽  
X. Li ◽  
C. Isherwood ◽  
...  
Keyword(s):  
2006 ◽  
Vol 291 (2) ◽  
pp. E282-E290 ◽  
Author(s):  
Riikka Lautamäki ◽  
Ronald Borra ◽  
Patricia Iozzo ◽  
Markku Komu ◽  
Terho Lehtimäki ◽  
...  

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.


Diabetologia ◽  
2005 ◽  
Vol 48 (11) ◽  
pp. 2282-2291 ◽  
Author(s):  
N. Stefan ◽  
F. Machicao ◽  
H. Staiger ◽  
J. Machann ◽  
F. Schick ◽  
...  

2014 ◽  
Vol 307 (7) ◽  
pp. G760-G768 ◽  
Author(s):  
D. P. Macfarlane ◽  
P. J. Raubenheimer ◽  
T. Preston ◽  
C. D. Gray ◽  
M. E. Bastin ◽  
...  

To investigate the potential of therapies which reduce glucocorticoid action in patients with Type 2 diabetes we performed a randomized, double-blinded, placebo-controlled crossover study of acute glucocorticoid blockade, using the glucocorticoid receptor antagonist RU38486 (mifepristone) and cortisol biosynthesis inhibitor (metyrapone), in 14 men with Type 2 diabetes. Stable isotope dilution methodologies were used to measure the rates of appearance of glucose, glycerol, and free fatty acids (FFAs), including during a low-dose (10 mU·m −2·min−1) hyperinsulinemic clamp, and subgroup analysis was conducted in patients with high or low liver fat content measured by magnetic resonance spectroscopy ( n = 7/group). Glucocorticoid blockade lowered fasting glucose and insulin levels and improved insulin sensitivity of FFA and glycerol turnover and hepatic glucose production. Among this population with Type 2 diabetes high liver fat was associated with hyperinsulinemia, higher fasting glucose levels, peripheral and hepatic insulin resistance, and impaired suppression of FFA oxidation and FFA and glycerol turnover during hyperinsulinemia. Glucocorticoid blockade had similar effects in those with and without high liver fat. Longer term treatments targeting glucocorticoid action may be useful in Type 2 diabetes with and without fatty liver.


Diabetes Care ◽  
2013 ◽  
Vol 37 (1) ◽  
pp. 242-251 ◽  
Author(s):  
Niina Matikainen ◽  
Leonie H. Bogl ◽  
Antti Hakkarainen ◽  
Jesper Lundbom ◽  
Nina Lundbom ◽  
...  

Obesity ◽  
2007 ◽  
Vol 15 (2) ◽  
pp. 531-538 ◽  
Author(s):  
Claus Thamer ◽  
Juergen Machann ◽  
Norbert Stefan ◽  
Michael Haap ◽  
Silke Schäfer ◽  
...  

2007 ◽  
Vol 92 (8) ◽  
pp. 3052-3059 ◽  
Author(s):  
Niina Matikainen ◽  
Sakari Mänttäri ◽  
Jukka Westerbacka ◽  
Satu Vehkavaara ◽  
Nina Lundbom ◽  
...  

Abstract Context/Objective: Postprandial lipemia and low adiponectin represent novel risk factors for vascular disease. This study aimed to determine whether liver fat content and adiponectin are predictors of postprandial triglyceride (TG)-rich lipoproteins (TRL). Patients/Interventions: Twenty-nine men were allocated into subgroups with either low (≤5%) or high (&gt;5%) liver fat measured with magnetic resonance proton spectroscopy. Subjects underwent an oral fat tolerance test with measurements of postprandial TG, cholesterol, apolipoprotein B-48 (apoB-48), and apoB-100 in TRL fractions, a euglycemic hyperinsulinemic clamp, and determination of abdominal fat volumes by magnetic resonance imaging. Results: Subjects with high liver fat displayed increased response of postprandial lipids in plasma, chylomicron, and very-low-density lipoprotein 1 (VLDL1) (Svedberg flotation rate 60–400) fractions. Liver fat correlated positively with postprandial responses (area under the curve) of TG (r = 0.597; P = 0.001), cholesterol (r = 0.546; P = 0.002), apoB-48 (r = 0.556; P = 0.002), and apoB-100 (r = 0.42; P = 0.023) in the VLDL1 fraction. Respective incremental areas under the curve correlated significantly with liver fat. Fasting adiponectin levels were inversely correlated with both postprandial lipids and liver fat content. Liver fat remained the only independent correlate in a multiple linear regression analysis for chylomicron and VLDL1 responses. Conclusions: Liver fat content is a close correlate of postprandial lipids predicting the responses of TRL in chylomicrons and VLDL1 better than measures of glucose metabolism or body adiposity. Low adiponectin concentration is closely linked to high liver fat content and impaired TRL metabolism. High liver fat content associated with postprandial lipemia represents potential risk factors for cardiovascular disease.


2011 ◽  
Vol 35 (5) ◽  
pp. 1112-1118 ◽  
Author(s):  
Vasco Herédia ◽  
Miguel Ramalho ◽  
Rafael O.P. de Campos ◽  
Brian Dale ◽  
Rafael Azevedo ◽  
...  

Nutrients ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 1314 ◽  
Author(s):  
Andras Franko ◽  
Dietrich Merkel ◽  
Marketa Kovarova ◽  
Miriam Hoene ◽  
Benjamin Jaghutriz ◽  
...  

Fatty liver is tightly associated with insulin resistance and the development of type 2 diabetes. I148M variant in patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene is associated with high liver fat but normal insulin sensitivity. The underlying mechanism of the disassociation between high liver fat but normal insulin sensitivity remains obscure. We investigated the effect of I148M variant on hepatic lipidome of subjects with or without fatty liver, using the Lipidyzer method. Liver samples of four groups of subjects consisting of normal liver fat with wild-type PNPLA3 allele (group 1); normal liver fat with variant PNPLA3 allele (group 2); high liver fat with wild-type PNPLA3 allele (group 3); high liver fat with variant PNPLA3 allele (group 4); were analyzed. When high liver fat to normal liver fat groups were compared, wild-type carriers (group 3 vs. group 1) showed similar lipid changes compared to I148M PNPLA3 carriers (group 4 vs. group 2). On the other hand, in wild-type carriers, increased liver fat significantly elevated the proportion of specific DAGs (diacylglycerols), mostly DAG (FA18:1) which, however, remained unchanged in I148M PNPLA3 carriers. Since DAG (FA18:1) has been implicated in hepatic insulin resistance, the unaltered proportion of DAG (FA18:1) in I148M PNPLA3 carriers with fatty liver may explain the normal insulin sensitivity in these subjects.


Diabetes ◽  
2007 ◽  
Vol 56 (8) ◽  
pp. 1960-1968 ◽  
Author(s):  
Maria Kolak ◽  
Jukka Westerbacka ◽  
Vidya R. Velagapudi ◽  
Dick Wågsäter ◽  
Laxman Yetukuri ◽  
...  

Author(s):  
María Correa‐Rodríguez ◽  
Mikel Izquierdo ◽  
Antonio García‐Hermoso ◽  
Robinson Ramírez‐Vélez

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