β-very low density lipoprotein induces triglyceride accumulation through receptor mediated endocytotic pathway in 3T3-L1 adipocytes

Yano, Toshihiro; Kobori, Shozo; Sakai, Masakazu; Anami, Yoshichika; Matsumura, Takeshi; Makino, Hírofumi; Kasho, Masaya; Shichiri, Motoaki

doi:10.1016/s0021-9150(97)00146-9

Cited by 14 publications

(7 citation statements)

References 27 publications

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“…Thus, the concomitant administration of E and FF did not have additive effects, suggesting that E may suppress the lipid‐lowering function of FF. Our data showed strong correlations among serum triglycerides, body weight, and WAT mass on treatment with E and FF in high‐fat diet‐fed female OVX mice, which is supported by findings that WAT lipids are derived largely from serum triglycerides (39)(40)(41).…”

Section: Discussionsupporting

confidence: 82%

Inhibition of the Actions of Peroxisome Proliferator‐activated Receptor α on Obesity by Estrogen

Jeong

Yoon

2007

Obesity

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JEONG, SUNHYO AND MICHUNG YOON. Inhibition of the actions of peroxisome proliferator-activated receptor ␣ on obesity by estrogen. Obesity. 2007;15:1430 -1440. Objective: To determine whether the major ovarian factor estrogen modulates peroxisome proliferator-activated receptor (PPAR) ␣ actions on obesity and to investigate the mechanism by which estrogen regulates PPAR␣ actions. Research Methods and Procedures: Female ovariectomized mice were randomly divided into four groups (n ϭ 8/group). After they were treated with combinations of high fat, fenofibrate (FF), or 17␤-estradiol (E) for 13 weeks, variables and determinants of obesity and lipid metabolism were measured using in vivo and in vitro approaches. Results: When female ovariectomized mice were given a high-fat diet with either FF or E, body weight gain and white adipose tissue mass were significantly reduced and serum lipid profiles were improved compared with control mice fed a high-fat diet alone. When mice were concomitantly treated with FF and E, however, E reversed the effects of FF on body weight gain, serum lipid profiles, and hepatic PPAR␣ target gene expression. Consistent with the in vivo data, E not only decreased basal levels of PPAR␣ reporter gene activation but also significantly decreased Wy14,643-induced luciferase reporter activity. In addition, inhibition of PPAR␣ functions by E did not seem to occur by interfering with the DNA binding of PPAR␣. Discussion: Our results demonstrate that in vivo and in vitro treatment of estrogen inhibited the actions of FFactivated PPAR␣ on obesity and lipid metabolism through changes in the expression of PPAR␣ target genes, providing evidence that FF does not regulate obesity in female mice with functioning ovaries.

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Section: Discussionsupporting

confidence: 82%

Inhibition of the Actions of Peroxisome Proliferator‐activated Receptor α on Obesity by Estrogen

Jeong

Yoon

2007

Obesity

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“…Plasma triglyceride levels were significantly suppressed in these animals, and yet, three-to fourfold renal cortical triglyceride elevations were observed. Cellular triglyceride levels reflect a balance between synthesis, substrate catabolism, and possible endocytic transport across the plasma membrane [19][20][21][22][23][24][25]. The available data suggest that multiple mechanisms, rather than any single pathway, likely account for the presently documented injury-induced renal triglyceride loading state.…”

Section: Discussionmentioning

confidence: 99%

Renal tubular triglyercide accumulation following endotoxic, toxic, and ischemic injury

Zager

Johnson

Hanson

2005

Kidney International

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Diverse forms of renal injury induce dramatic triglyceride loading in proximal tubules/renal cortex, suggesting that this is a component of a cell stress response. PLA(2) activity, increased triglyceride/triglyceride substrate (e.g., fatty acid) uptake, and possible systemic cytokine (e.g., from LPS) stimulation, may each contribute to this result. Finally, in addition to being a marker of prior cell injury, accumulation of triglyceride (or of its constituent fatty acids) may predispose tubules to superimposed ATP depletion or oxidant attack.

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“…A recent study suggests that uptake of VLDL by adipocytes stimulates intracellular lipid accumulation [50]. To identify if either HSPG or LDL receptor family members play a role in this process, we incubated mature adipocytes with DiI-labeled apoE-enriched VLDL in the presence or absence of either heparin (to inhibit HSPG activity) or RAP (to inhibit VLDL-R and LRP function) and visualized the cells by fluorescence microscopy (Fig.…”

Section: Resultsmentioning

confidence: 99%

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et al. 2005

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BackgroundTransport of fatty acids within the cytosol of adipocytes and their subsequent assimilation into lipid droplets has been thoroughly investigated; however, the mechanism by which fatty acids are transported across the plasma membrane from the extracellular environment remains unclear. Since triacylglycerol-rich lipoproteins represent an abundant source of fatty acids for adipocyte utilization, we have investigated the expression levels of cell surface lipoprotein receptors and their functional contributions toward intracellular lipid accumulation; these include very low density lipoprotein receptor (VLDL-R), low density lipoprotein receptor-related protein (LRP), and heparan sulfate proteoglycans (HSPG).ResultsWe found that expression of these three lipoprotein receptors increased 5-fold, 2-fold, and 2.5-fold, respectively, during adipocyte differentiation. The major proteoglycans expressed by mature adipocytes are of high molecular weight (>500 kD) and contain both heparan and chondroitin sulfate moieties. Using ligand binding antagonists, we observed that HSPG, rather than VLDL-R or LRP, play a primary role in the uptake of DiI-lableled apoE-VLDL by mature adipocytes. In addition, inhibitors of HSPG maturation resulted in a significant reduction (>85%) in intracellular lipid accumulation.ConclusionsThese results suggest that cell surface HSPG is required for fatty acid transport across the plasma membrane of adipocytes.

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β-very low density lipoprotein induces triglyceride accumulation through receptor mediated endocytotic pathway in 3T3-L1 adipocytes

Cited by 14 publications

References 27 publications

Inhibition of the Actions of Peroxisome Proliferator‐activated Receptor α on Obesity by Estrogen

Inhibition of the Actions of Peroxisome Proliferator‐activated Receptor α on Obesity by Estrogen

Renal tubular triglyercide accumulation following endotoxic, toxic, and ischemic injury

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