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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined whether fatty liver, as diagnosed with abdominal ultrasonography, is an independent risk factor for diabetes mellitus during 10 years of follow-up. A total of 840 subjects (467 men and 373 women) were followed for the entire 10 years. The criteria for being non-diabetic were having no history of diabetes, having a fasting plasma glucose level of less than 110 mg/dl and a serum hemoglobin A1c level of 6.4% or less. We indicated that every examine received all examinations after 12 hours of fasting. Well-trained technicians performed abdominal ultrasonography. Although univariate analysis revealed that the presence of fatty liver was related to hyperglycemia 10 years later, multiple logistic regression analysis did not support this finding. In the multiple logistic regression analysis fasting plasma glucose levels at the baseline and age were significantly related to hyperglycemia (odds ratio [OR] = 1.16, 95% confidence interval [CI]: 1.11-1.21, OR = 1.07, 95% CI: 1.01-1.14, respectively). Fatty liver was not an independent risk factor for hyperglycemia in our follow-up study 10 years after the first diagnosis. The high fasting plasma glucose levels were a risk factor for diabetes, even in the normal range.
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PMID:The association of fatty liver and diabetes risk. 1258 9

In this review, the microarray technology and especially oligonucleotide arrays are exemplified with a practical example taken from the perilipin-/- mice and using the dChip software, available for non-lucrative purposes. It was found that the liver of perilipin-/- mice was healthy and normal, even under high-fat diet when compared with the results published for the scd1-/- mice, which under high-fat diets had a darker liver, suggestive of hepatic steatosis. Scd1 is required for the biosynthesis of monounsaturated fatty acids and plays a key role in the hepatic synthesis of triglycerides and of very-low-density lipoproteins. Both models of obesity resistance share many similar phenotypic antiobesity features, however, the perilipin-/- mice had a significant downregulation of stearoyl CoA desaturases scd1 and scd2 in its white adipose tissue, but a normal level of both genes inside the liver, even under high-fat diet. Here, different microarray methodologies are discussed, and also some of the most recent discoveries and perspectives regarding the use of microarrays, with an emphasis on obesity gene expression, and a personal remark on my findings of increased expression for hemoglobin transcripts and other hemo related genes (hemo-like), and for leukocyte like (leuko-like) genes inside the white adipose tissue of the perilipin-/- mice. In conclusion, microarrays have much to offer in comparative studies such as those in antiobesity, and also they are methodologies adequate for new astounding molecular discoveries [free full text of this article Online].
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PMID:Microarrays, antiobesity and the liver. 1565 55

To increase our understanding of the effect of thiazolidinediones, a new class of antidiabetic drugs, on liver function as well as glycemic control, we investigated liver function before, during, and after treatment with troglitazone and pioglitazone. A total of 32 patients with type 2 diabetes were studied. Glycemic control and liver function were measured before, during, and after 4 to 12 weeks of treatment with troglitazone or pioglitazone. Glycemic control was assessed by fasting levels of plasma glucose, hemoglobin A 1c , and serum insulin, and liver function was assessed by asparatate aminotransferase (AST), alanine aminotransferase (ALT), and gamma -glutamyl transpeptidase ( gamma-GTP). Homeostasis model assessment for insulin resistance was used as an index of insulin resistance. During treatment with troglitazone, fasting plasma glucose and hemoglobin A 1c levels and homeostasis model assessment for insulin resistance were significantly decreased. Serum AST, ALT, and gamma-GTP levels were significantly decreased during treatment (AST, -17.4%; ALT, -27.2%; gamma-GTP, -47.9%) and returned to pretreatment levels after 4 weeks of withdrawal of the drug. A similar tendency was observed during treatment with pioglitazone (AST, -4.7%; ALT, -16.4%; gamma-GTP, -30.8%). These data suggest that, in contrast to the deterioration of liver function reported in a small subset of patients treated with troglitazone, treatment with thiazolidinediones was associated with a decrease in serum transaminases in most patients. The improvement in liver function parameters known to be associated with fatty liver in the present study, together with an improvement in fatty liver reported for another class of insulin sensitizers, biguanides, suggests that thiazolidinediones may have a beneficial effect on fatty liver.
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PMID:Improvement of liver function parameters in patients with type 2 diabetes treated with thiazolidinediones. 1579 62

Glycated hemoglobin (GHb) measured as HbA1c in diabetic patients, is used to evaluate long-term control of diabetes mellitus, and most accurately reflects the previous 2-3 months of glycemic control. Liver disease is one of the leading causes of death in persons with type 2 diabetes mellitus. Diabetic patients can present with abnormal liver chemistries, from benign nonalcoholic fatty liver disease to severe cirrhosis of the liver. Because liver disease is associated with impaired glucose tolerance and diabetes mellitus, tools are needed to measure long-term glycemic control. In this review we discuss current information on glycated hemoglobin, HbA1c assay methods, attempts to standardize HbA1c assay methods, fructosamine and interferences caused by liver disease. We aim to alert the reader to current problems in determining long-term glycemic control parameters, HbA1c and fructosamine, and describe the measures necessary for proper interpretation of HbA1c.
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PMID:Glycated hemoglobin and liver disease in diabetes mellitus. 1639 39

Congenital generalized lipodystrophy (CGL) is a disease characterized by generalized lack of body fat, insulin resistance, hypertriglyceridemia, and fatty liver. We studied the long-term effects of recombinant human insulin-like growth factor I (rhIGF-I) treatment on glucose and lipid metabolism and the growth in a patient with CGL. During rhIGF-I treatment, the serum triglyceride level was maintained almost within the normal range, and the plasma glycosylated hemoglobin A1c (HbA1c) levels were maintained under 8.0% (5.8%-7.9%). Thus, rhIGF-I treatment was effective in lowering glucose and triglyceride levels over the long-term in a CGL patient. However, it was difficult to suppress the patient's voracious appetite. Although serum total IGF-I levels were extremely high (1000-1700 ng/ml), growth was not accelerated after the start of rhIGF-I treatment, likely because of normal IGF binding protein 3 (IGFBP-3) levels. During rhIGF-I treatment, the patient developed a recurrence of mild hypertrophic cardiomyopathy and a mild elevation of intraocular pressure.
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PMID:Long-term effects of recombinant human insulin-like growth factor I treatment on glucose and lipid metabolism and the growth of a patient with congenital generalized lipodystrophy. 1690 64

The present study examined a new model of impaired glucose tolerance (IGT) in a nonhuman primate fed with a high-fructose and high-fat (HFF) diet that contained 15% lard, 31% fructose, and 1% cholesterol. Female cynomolgus monkeys (age, 3-4 years) were divided into two groups: 1) those fed with normal control diet (N = 5) and 2) those fed with HFF diet (N = 5). In the HFF diet group, total cholesterol and low-density lipoprotein cholesterol in blood were significantly increased four- to fivefold when compared with the normal control diet group. No difference in the blood glucose, insulin, hemoglobin A1c, and triglyceride levels was detected between the two groups. Plasma levels of adiponectin, but not of resistin, were significantly higher in HFF diet at 20 weeks after HFF diet feeding. Oral glucose tolerance test was performed before HFF diet feeding and at 12 and 24 weeks after HFF diet feeding, but no significant changes in glucose sensitivity were observed even 24 weeks after HFF diet feeding. Twenty-four weeks after HFF diet feeding, accumulated foam cells and infiltrated macrophages were histologically detected in the thoracic aorta, in addition to a fatty liver. Interestingly, the pancreatic beta cells appeared normal in the HFF diet group. These results show that a chronic HFF diet does not induce IGT but can cause atherosclerotic lesions in conjunction with the generation of a fatty liver phenotype in cynomolgus monkey; however, the present results are very preliminary and they need to be validated in larger-scale studies in the future.
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PMID:Effect of fructose-rich high-fat diet on glucose sensitivity and atherosclerosis in nonhuman primate. 1720 Jul 27

Patients with chronic hepatitis C frequently have serum and hepatic iron overload, but the mechanism is unknown. Recently identified hepcidin, exclusively synthesized in the liver, is thought to be a key regulator for iron homeostasis and is induced by infection and inflammation. This study was conducted to determine the hepatic hepcidin expression levels in patients with various liver diseases. We investigated hepcidin mRNA levels of liver samples by real-time detection-polymerase chain reaction; 56 were hepatitis C virus (HCV) positive, 34 were hepatitis B virus (HBV) positive, and 42 were negative for HCV and HBV (3 cases of auto-immune hepatitis, 7 alcoholic liver disease, 13 primary biliary cirrhosis, 9 nonalcoholic fatty liver disease, and 10 normal liver). We analyzed the relation of hepcidin to clinical, hematological, histological, and etiological findings. Hepcidin expression levels were strongly correlated with serum ferritin (P < 0.0001) and the degree of iron deposit in liver tissues (P < 0.0001). Hepcidin was also correlated with hematological parameters (vs. hemoglobin, P = 0.0073; vs. serum iron, P = 0.0012; vs. transferrin saturation, P < 0.0001) and transaminase levels (P = 0.0013). The hepcidin-to-ferritin ratio was significantly lower in HCV(+) patients than in HBV(+) patients (P = 0.0129) or control subjects (P = 0.0080). In conclusion, hepcidin expression levels in chronic liver diseases were strongly correlated with either the serum ferritin concentration or degree of iron deposits in the liver. When adjusted by either serum ferritin values or hepatic iron scores, hepcidin indices were significantly lower in HCV(+) patients than in HBV(+) patients, suggesting that hepcidin may play a pivotal role in the pathogenesis of iron overload in patients with chronic hepatitis C.
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PMID:Hepcidin expression in the liver: relatively low level in patients with chronic hepatitis C. 1751 61

High levels of myocardial and hepatic triglyceride are common in obesity and type 2 diabetes. Monotherapy with thiazolidinedione agents reduces hepatic steatosis by up to 50% in patients with type 2 diabetes. It is not known if treatment with a thiazolidinedione added to insulin has a similar beneficial antisteatotic effect. The aim of our study was to determine whether the addition of pioglitazone to insulin treatment in patients with type 2 diabetes has antisteatotic action in the heart and the liver. Thirty-two patients were randomized to 6 months of treatment with insulin or insulin plus pioglitazone. In addition to blood tests, we evaluated myocardial and hepatic triglyceride content, as well as subcutaneous and visceral fat mass at the L2 level, by magnetic resonance spectroscopy and imaging, respectively. Despite weight and subcutaneous fat mass gain, hemoglobin A1c was significantly reduced by both treatments. Myocardial and hepatic triglyceride contents were reduced by the treatment with pioglitazone plus insulin (p = .02 and .03, respectively) but not by the treatment with insulin. Systolic and diastolic blood pressure and heart function remained unchanged in both groups. The addition of pioglitazone to insulin therapy reduced myocardial and hepatic steatosis, consistent with the reported ability of the thiazolidinedione agents to redistribute fat from nonadipose to subcutaneous adipose depots.
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PMID:Effect of pioglitazone therapy on myocardial and hepatic steatosis in insulin-treated patients with type 2 diabetes. 1785 Jul 34

It is unknown whether chronic kidney disease (CKD) is associated with nonalcoholic fatty liver disease among patients with type 2 diabetes. We followed 1760 outpatients with type 2 diabetes and normal or near-normal kidney function and without overt proteinuria for 6.5 yr for the occurrence of CKD (defined as overt proteinuria and/or estimated GFR <60 ml/min per 1.73 m(2)). During follow-up, 547 participants developed incident CKD. Nonalcoholic fatty liver disease, diagnosed by liver ultrasound and exclusion of other common causes of chronic liver disease, was associated with a moderately increased risk for CKD (hazard ratio 1.69; 95% confidence interval 1.3 to 2.6; P < 0.001). Adjustments for gender, age, body mass index, waist circumference, BP, smoking, diabetes duration, glycosylated hemoglobin, lipids, baseline estimated GFR, microalbuminuria, and medications (hypoglycemic, lipid-lowering, antihypertensive, or antiplatelet drugs) did not appreciably attenuate this association (hazard ratio 1.49; 95% confidence interval 1.1 to 2.2; P < 0.01). In conclusion, our findings suggest that nonalcoholic fatty liver disease is associated with an increased incidence of CKD in individuals with type 2 diabetes, independent of numerous baseline confounding factors.
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PMID:Increased risk of CKD among type 2 diabetics with nonalcoholic fatty liver disease. 1838 24

To investigate how liver disease alter the serum glycated proteins as markers of diabetic control, we studied serum GA, A1c and especially GA/A1c ratio in 255 patients having over 35IU/L in ALT(transaminase) compared with those of 829 type 2 diabetes mellitus (DM) in cross sectional manner. 255 patients with liver diseases were divided into 69 patients with biopsy proven liver cirrhosis (LC), 66 patients with chronic hepatitis(CH) and 120 patients with fatty liver(FL) diagnosed by abdominal echography. The mean GA/A1c ratio (+/-SD) was significantly higher (p<0.0001) in LC group(3.71+/-1.03) than the other groups (3.03+/-0.45 for CH, 3.05+/-0.42 for DM), while the mean GA/A1c ratio in FL group was significantly lower(2.74+/-0.31) (p<0.0001)) than that of DM groups. In LC group the GA/A1c ratio increased significantly depending upon serum albumin and/or platelet reductions. The GA/A1c ratio was significantly correlated with the other laboratory data such as serum albumin, cholinesterase, total cholesterol levels and weakly correlated with serum hemoglobin level. We also followed the serum levels of GA and A1c and the GA/A1c ratio during about 13 months (5 times blood collections) in 18 patients enrolled in this study. Resultantly the coefficient of variation of GA/A1c ratio was the smaller than the others(GA, A1c). The ROC curve of GA/A1c ratio for LC versus FL group was the most reliable between four groups and the cut-off value for LC versus FL was 2.94. Theses results suggest that GA/A1c ratio could be an useful marker for different diagnosis when facing patients with abnormal serum ALT level in a clinical setting.
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PMID:[Relationship between glycated albumin (GA) and glycated hemoglobin (A1c) in 255 patients with liver diseases using cross-sectional laboratory data]. 1897 54


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