Apolipoprotein A1 expression in young and aged rats is modulated by dietary carbohydrates

Mooradian, Arshag D.; Wong, Norman C.; Shah, Gul N.

doi:10.1016/s0026-0495(97)90204-3

Cited by 19 publications

(11 citation statements)

References 12 publications

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“…The reduced expression of apo A-I in obese type 2 diabetic subjects, despite the increased levels of plasma insulin, cannot be simply attributed to insulin resistance. Thus, insulin resistance and hyperinsulinemia induced with a high-fructose diet in rats is associated with increased apo A-I levels (56). Similarly, aging in rats is associated with increased expression of apo A-I, although it is accompanied with insulin resistance (57).…”

Section: Effect Of Insulin Resistance On Apo A-i Expressionmentioning

confidence: 99%

Transcriptional Control of Apolipoprotein A-I Gene Expression in Diabetes

2004

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Cardiovascular disease continues to be the leading cause of mortality in diabetes. One of the factors contributing to the increased risk is the high prevalence rate of low plasma concentrations of HDL cholesterol. Multiple potential mechanisms account for the cardioprotective effects of HDL and its main protein apolipoprotein (apo) A-I. The reduced plasma concentrations of HDL could be the result of increased fractional clearance of HDL and reduced expression of apo A-I. In animal models of diabetes and in cell cultures treated with high concentrations of glucose, apo A-I expression is reduced. In this review we will discuss the alterations in transcriptional control of apo A-I in diabetes. The role of select nutritional and hormonal alterations commonly found in diabetes will be reviewed. Specifically, we will review the literature on the effect of hyperglycemia, hypoinsulinemia, and ketoacidosis, as well as the role of various mediators of insulin resistance, such as fatty acids, cytokines, and prostanoids, on apo A-I promoter activity. Identifying the mechanisms that modulate apo A-I gene expression will aid in the new development of therapeutic agents that increase plasma apo A-I and HDL concentrations.

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Section: Effect Of Insulin Resistance On Apo A-i Expressionmentioning

confidence: 99%

Transcriptional Control of Apolipoprotein A-I Gene Expression in Diabetes

2004

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“…The specificity of the polyclonal apoAI antiserum and the method of its preparation have been described previously (Mooradian et al 1997). Plasma protein samples (5 µg) were electrophoresed in a 10% sodium dodecylsulfate (SDS)-polyacrylamide gel (Laemmli 1970), and transferred electrophoretically to a nitrocellulose membrane (Towbin et al 1979).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…Hep G2 liver cells and Caco-2 intestinal cells were transfected with the plasmid pA1·474.CAT, which carries the full sequence of rat apoAI gene promoter, along with the CAT reporter gene (Widom et al 1991, Romney et al 1992, Taylor et al 1996, Mooradian et al 1997, Harnish et al 1998, Murao et al 1998. Both of these cell lines are suitable for these studies since they express the endogenous apoA1 gene (see below).…”

Section: Effect Of Ketone Bodies On the Apoa1 Gene Promotermentioning

confidence: 99%

Effects of ketoacidosis on rat apolipoprotein A1 gene expression: a link with acidosis but not with ketones

Haas¹,

Pun²,

Reinacher³

et al. 2000

Journal of Molecular Endocrinology

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To determine if ketoacidosis contributes to reduced apolipoprotein A1 (apoA1) expression in insulindeficient diabetic rats, we examined the regulation of apoA1 gene expression in response to changes in ambient pH or ketone body concentrations. Hepatic apoAI mRNA levels were reduced 42% in diabetic rats relative to nondiabetic controls (means ..; 321·8 43·7 vs 438·7 58·8 arbitrary units; P<0·03). Neither endogenous apoA1 mRNA nor transcriptional activity of the rat apoA1 gene promoter (from 474 to 7) were altered by sodium butyrate or isobutyramide (0·3 mM to 10 mM) in Hep G2 or Caco-2 cells. Rat hepatic and intestinal apoA1 mRNA levels, and plasma apoA1 concentration, were not altered 24 h after isobutyramide administration (500 mg/kg by gavage). When the effect of altering ambient pH within a wide range commonly encountered in vivo was studied, acidosis (pH 6·7), relative to alkalosis (pH 7·9), decreased apoAI mRNA levels relative to glyceraldehyde-3-phosphate dehydrogenase mRNA by 47% in Hep G2 cells (P<0·025) and by 24% in Caco-2 cells (P<0·017). Acidosis did not alter cytomegalo virus (CMV)--galactosidase activity, or the activity of the simian virus (SV40) early-region promoter, in either cell line transfected with the respective constructs. The lowering of ambient pH was associated with a graded reduction in apoAI promoter activity. At pH 6·7, apoAI promoter activity was reduced by 75% compared with promoter activity at pH 7·9. These observations indicate that acidosis, but not ketosis, contributes to the reduction in apoA1 expression during diabetic ketoacidosis by down-regulating apoAI promoter activity.

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“…It has been suggested that apo A1 and apo B are the sensitive biomarkers of cardiovascular disease. Reduced plasma HDL due to the inhibition of apo A1 synthesis may contribute to the increased incidence of coronary heart disease in diabetes (Haffner et al, 1998;Mooradian et al, 1997;Solymoss et al, 1995). Epidemiological studies suggest that apo A1 and HDL have cardioprotective properties, presumably because of their roles in reverse cholesterol transport (RCT) (Franceschini et al, 1991).…”

Section: Experimental Groupmentioning

confidence: 99%

Ethanol extract ofButea monospermabark modulates dyslipidemia in streptozotocin-induced diabetic rats

Divya

Mini

2014

Pharmaceutical Biology

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Context: Dyslipidemia is one of the major risk factors for cardiovascular disease in diabetes mellitus (DM). The availability of multiple lipid-lowering drugs and supplements provides new opportunities for patients to regulate lipid levels. Objective: The present study was designed to evaluate the effect of Butea monosperma Lam. (Fabaceae) bark extract in diabetes-induced dyslipidemia. Materials and methods: A daily dose of B. monosperma bark extract (BMBE, 500 mg/kg body weight) was given orally to streptozotocin (STZ)-induced diabetic rats for 60 d. Several indices such as blood glucose, insulin, glycosylated hemoglobin, TC, TG, high-density lipoproteincholesterol (HDL-C), apo A1, apo B, activities of lipogenic enzymes in tissues, liver function tests, and histopathology of liver were analyzed to assess the modulation of STZ-induced diabetic dyslipidemia by B. monosperma bark. Results: BMBE significantly reduced blood glucose (40.79%) and increased plasma insulin (37.5%) levels in diabetic rats. Altered levels of serum lipids, lipoproteins, and activities of lipogenic enzymes in tissues were partially restored upon the administration of BMBE in diabetic rats. Liver function tests and histopathological examination revealed that consumption of BMBE at a dose of 500 mg/kg body weight had no toxic effects in experimental rats. Conclusion: The findings suggest that BMBE supplementation could ameliorate dyslipidemia in DM.

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Apolipoprotein A1 expression in young and aged rats is modulated by dietary carbohydrates

Cited by 19 publications

References 12 publications

Transcriptional Control of Apolipoprotein A-I Gene Expression in Diabetes

Transcriptional Control of Apolipoprotein A-I Gene Expression in Diabetes

Effects of ketoacidosis on rat apolipoprotein A1 gene expression: a link with acidosis but not with ketones

Ethanol extract ofButea monospermabark modulates dyslipidemia in streptozotocin-induced diabetic rats

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