Differential Expression of Lipoprotein Lipase Gene in Tissues of the Rat Model with Visceral Obesity and Postprandial Hyperlipidemia

Hikita, Minoru; Bujo, Hideaki; Yamazaki, Kenya; Taira, Kouichi; Takahashi, Kazuo; Kobayashi, Junji; Saitō, Yasushi

doi:10.1006/bbrc.2000.3695

Cited by 21 publications

(11 citation statements)

References 38 publications

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“…It is also of interest to note that bezafi brate reduced the LDL-C level after 24 h (Table I), but not after 7 h. Furthermore, other plasma lipid levels were not signifi cantly changed indicating that bezafi brate has an acute lowering activity only on plasma triglycerides and LDL-C. This is concomitant with the mechanism of action of fi brates (Fujiwara et al, 1997;Yamada, 1997;Norioka et al, 2000;Nagai et al, 2000;Hikita et al, 2000) whose LDL-C-lowering activity is not strongly marked, but their triglycerides-decreasing effect is very spectacular especially by stimulation of gene expression of lipoprotein lipase leading to enhanced catabolism of VLDL, synthesis of fatty acids and reduced VLDL secretion.…”

Section: Discussionmentioning

confidence: 84%

Pharmacological Evaluation of Novel Indole-2-carboxamides As Potent Lipid-Lowering Agents in Triton-WR-1339-Induced Hyperlipidemic Rats

Al-Qirim

Shahwan

Shattat

et al. 2009

Zeitschrift Für Naturforschung C

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The lipid-lowering effects of two novel antihyperlipidemic agents, BMI2C [N-(4-benzoylphenyl)-5-methoxy-1H-indole-2-carboxamide] and DDMI2C [N-(9,10-dihydro-9,10-dioxoanthracen-2-yl)-5-methoxy-1H-indole-2-carboxamide], were studied using hyperlipidemic rats as an experimental model; hyperlipidemia was developed by intraperitoneal injection of Triton WR-1339 (200 mg/kg body weight). At a dose of 15 mg/kg body weight, BMI2C and DDMI2C signifi cantly reduced elevated plasma triglyceride levels after 7 and 24 h. Furthermore, BMI2C and DDMI2C signifi cantly reduced elevated plasma total cholesterol levels after 24 h. Interestingly, high-density lipoprotein-cholesterol levels were signifi cantly increased in all treated groups. These fi ndings indicate that the two studied novel compounds have a promising potential in the treatment of hyperlipidemia and atherosclerosis. Key words: BMI2C [N-(4-Benzoylphenyl)-5-methoxy-1H-indole-2-carboxamide], DDMI2C[N-(9,10-Dihydro-9,10-dioxoanthracen-2-yl)-5-methoxy-1H-indole-2-carboxa mide], Antihyperlipidemic Activity

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Section: Discussionmentioning

confidence: 84%

Pharmacological Evaluation of Novel Indole-2-carboxamides As Potent Lipid-Lowering Agents in Triton-WR-1339-Induced Hyperlipidemic Rats

Al-Qirim

Shahwan

Shattat

et al. 2009

Zeitschrift Für Naturforschung C

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“…Insulin is a major stimulator of the postprandial increase of LPL activity, but other reports have suggested that decreased LPL gene expression is mediated by the increase of insulin in rats with postprandial hyperlipidemia. 21,22) In addition, some recent transgenic or knockout mice studies have suggested a role of apolipoproteins, receptors for lipoproteins and other enzymes in the mechanisms of lipid abnormalities. Investigation of enzyme activities and/or the expression of these molecules in nateglinide-treated animals is planned to address these issues.…”

Section: )mentioning

confidence: 99%

Nateglinide Suppresses Postprandial Hypertriglyceridemia in Zucker Fatty Rats and Goto-Kakizaki Rats: Comparison with Voglibose and Glibenclamide.

Mine

Miura

Kitahara

et al. 2002

Biological & Pharmaceutical Bulletin

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“…In particular, the expression of LPL is an extremely sensitive marker for the insulin resistance-induced complications. In this context, we have shown that the negative correlation between the serum concentrations of TNF-a or insulin and the LPL mRNA expression in muscle and subcutaneous fat using the model rats for excessive visceral fat accumulation [10]. These results suggest that the amount of TNF-a secretion in adipocytes is one of the most distinct determinants for the difference of functions observed in subcutaneous and visceral fat tissues.…”

Section: Discussionmentioning

confidence: 76%

“…excessive visceral fat accumulation revealed negative correlation between the serum concentration of insulin or TNF-a and the LPL mRNA expression in muscle and subcutaneous fat [10]. These in vivo results strongly suggest that visceral fat secretes cytokines such as TNF-a, and that this mechanism is the cause of insulin resistance in human beings as well as rodents.…”

mentioning

confidence: 74%

Alterations of insulin sensitivity by the implantation of 3T3-L1 cells in nude mice. A role for TNF-α?

et al. 2002

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Visceral fat accumulation is known to be a clinical index for insulin resistance related to obesity [1±3]. Patients with excessive accumulation of visceral fat frequently suffered from metabolic disorders, such as hyperlipidaemia, hypertension and glucose intolerance [4±6]. However, molecular mechanisms for the pathogenesis of obesity-accompanied metabolic disorders are not clear. So far, it has been clarified that adipose cells in visceral areas have different functions both in vivo and in vitro from the cells in subcutaneous areas, and these differences might contribute the pathological significance of visceral fat accumulation for accompanying insulin resistance and hyperinsulinaemia [7]. We have reported that patients with excessive visceral fat accumulation show delayed postprandial triglyceride (TG) metabolism compared to normal subjects, and the disturbed metabolism is, at least in part, caused by reduced lipoprotein lipase (LPL) mass and activity in their sera [8,9]. In accordance with the clinical observations, model rats for Diabetologia (2002) Abstract Aims/hypothesis. Visceral adipocytes have different functions than those from the subcutaneous fat area. These differences could contribute to the pathological significance of excessive visceral fat accumulation for accompanying insulin resistance and hyperinsulinaemia. This study addresses this hypothesis and describes a unique method to clarify whether the functional differences between visceral and subcutaneous adipocytes depend on their anatomical location. Methods. 3T3-L1 cells or TNF-a overexpressing CHO cells were implanted into subcutaneous fat area or mesenteric area as visceral fat area in athymic mice of BALB/C strain. Then, serum insulin, glucose, TNF-a, and several markers of lipid metabolism were measured in the fasting condition. OGTT was also analysed.Results. During the course of glucose loading, the mice which had 3T3-L1 cells implanted into mesenteric area but not into subcutaneous fat area showed remarkably increased serum insulin and TMF-a concentrations, compared to the control mice. Moreover, serum insulin concentrations of the mice, implanted with TNF-a overexpressing cells into subcutaneous fat area, were apparently higher than that of control mice. Conclusion/interpretation. This method of implanting adipose cells into subcutaneous or visceral fat area showed high TNF-a concentration and insulin resistance by the adipose cells in visceral area of nude mice. Furthermore, we found that the functional significance of visceral fat accumulation for TNF-a-induced insulin resistance is partly caused by the interaction of adipocytes with surrounding conditions in mesenteric area. [Diabetologia (2002) 45:518±526]

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Differential Expression of Lipoprotein Lipase Gene in Tissues of the Rat Model with Visceral Obesity and Postprandial Hyperlipidemia

Cited by 21 publications

References 38 publications

Pharmacological Evaluation of Novel Indole-2-carboxamides As Potent Lipid-Lowering Agents in Triton-WR-1339-Induced Hyperlipidemic Rats

Pharmacological Evaluation of Novel Indole-2-carboxamides As Potent Lipid-Lowering Agents in Triton-WR-1339-Induced Hyperlipidemic Rats

Nateglinide Suppresses Postprandial Hypertriglyceridemia in Zucker Fatty Rats and Goto-Kakizaki Rats: Comparison with Voglibose and Glibenclamide.

Alterations of insulin sensitivity by the implantation of 3T3-L1 cells in nude mice. A role for TNF-α?

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