Specificity and Cross Reactivity in Bile Acid Radioimmunoassays Serum Bile Acids, Radioimmunoassay

1979 ◽  
Vol 12 (8) ◽  
pp. 927-933 ◽  
Author(s):  
D. G. Sampson ◽  
G. M. Murphy ◽  
L. M. Cross ◽  
D. Catty
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Cross Reactivity ◽  
Serum Bile Acids

Evaluation of a Commercial Enzymatic Method for the Determination of Total Serum Bile Acids

1980 ◽  
Vol 17 (6) ◽  
pp. 301-306 ◽  
Author(s):  
Per Tobiasson ◽  
Magnus Källberg
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Reference Range ◽  
Reference Value ◽  
Total Serum ◽  
Enzymatic Method ◽  
Normal Range ◽  
Serum Samples ◽  
Serum Bile Acids

An enzymatic method (Sterognost-3α® Flu, Nyegaard & Co, Oslo, Norway) for the determination of total serum bile acids has been evaluated, and reference values for fasting and postprandial total serum bile acids have been established. Precision was rather low in the lower normal range but satisfactory in the upper reference range and for elevated values. The upper reference value for fasting total serum bile acids was 5·0 μmol/l. Maximal postprandial elevations occurred at varying intervals after a test meal and the upper postprandial reference value was 12 μmol/l. Certain serum samples were also analysed by radioimmunological methods for conjugates of cholic and chenodeoxycholic acids. The values obtained with the enzymatic method correlated satisfactorily with those of the radioimmunoassay methods for most of the serum samples analysed. However, a number of samples with slightly elevated bile acid concentrations, as measured by the comparison radioimmunoassay methods, were found to have normal total serum bile acids when measured by the enzymatic method.

Abstract 296: Decreased Hepatic Avpr1a Gene Expression and Elevated Serum Bile Acid in Mouse Model of Metabolic Syndrome

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Xiaoya Ma ◽  
Peter F Bodary
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Bile Acid ◽  
Bile Acids ◽  
Serum Bile Acid ◽  
Hepatic Gene Expression ◽  
Serum Bile Acids ◽  
Kk Mice ◽  
The Metabolic Syndrome

The KK/HIJ mouse has been demonstrated to have polygenic obesity and insulin resistance and serve as a model of metabolic syndrome. From microarray studies in this mouse strain, we observed hepatic gene expression of arginine vasopressin receptor 1A (Avpr1a) as the most differentially elevated gene in the liver following 3-week of voluntary wheel running activity. Subsequent studies validated that hepatic Avpr1a gene expression is significantly upregulated following voluntary activity and also highly suppressed (4 to 8-fold) in 2 independent models of insulin resistance (including obesity and lipoatrophic models). Although Avpr1a is highly abundant in the liver, its physiologic role is not well described. One proposed role for hepatic Avpr1a is mediation of vasopressin-induced bile acid secretion. To further evaluate the relationship between hepatic Avpr1a and bile acid homeostasis, we determined the age-related change in these variables in female KK mice. To investigate, adipose tissue, liver and serum were collected from female KK mice from before sexual maturity (PRE: 4.5 weeks old, n=9) and after sexual maturation (POST: 6 to 30 weeks old, n=12). Consistent with previous studies using this obesity-prone strain, we observed a robust increase in adiposity with age despite a standard rodent chow diet. RT-PCR studies of hepatic gene expression revealed a 53% lower Avpr1a in POST compared to PRE mice (p<0.00001). In parallel with the drop in hepatic Avpr1a gene expression was an increase in serum bile acids (PRE: 26.56± 9.98μmol/L; POST: 39.40± 9.63μmol/L; p<0.01). A negative correlation was evident between hepatic Avpr1a gene expression and serum bile acid level (R= -0.51). The change in Avpr1a and bile acids was pronounced at the age of onset of estrous cycling. In conclusion, female KK mice have a significant increase in fat mass with age in parallel with an elevation of serum bile acids and downregulation of hepatic Avpr1a gene expression. We propose that suppression of hepatic Avpr1a increases hydrophobic bile acids in the liver and serum and promotes hepatic inflammation, contributing to symptoms of the metabolic syndrome.

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