Long-chain fatty acids decrease lipoprotein lipase activity of cultured rat adipocyte precursors

Kirkland, James L.; Hollenberg, C. H.; Kindler, Sarah; Roncari, Daniel A. K.

doi:10.1016/0026-0495(94)90236-4

Cited by 11 publications

(6 citation statements)

References 46 publications

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“…Previous studies have shown enhanced adipose tissue lipolysis in both normo‐ and hypoglycemic GSD Ia patients, 60,61 while TG hydrolysis activities were reduced under normoglycemia 42,44,53,56,67 . The fact that adipocyte lipolysis and VLDL catabolism are also altered in well‐controlled patients is most likely explained by the presence of insulin resistance associated with dietary overtreatment, 68 which also enhances adipose tissue lipolysis and circulating NEFA levels that may, in turn, inhibit VLDL catabolism 42,47‐49,69,70 …”

Section: Discussionmentioning

confidence: 97%

“… 42 , 44 , 53 , 56 , 67 The fact that adipocyte lipolysis and VLDL catabolism are also altered in well‐controlled patients is most likely explained by the presence of insulin resistance associated with dietary overtreatment, 68 which also enhances adipose tissue lipolysis and circulating NEFA levels that may, in turn, inhibit VLDL catabolism. 42 , 47 , 48 , 49 , 69 , 70 …”

Section: Discussionmentioning

confidence: 99%

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Impaired Very‐Low‐Density Lipoprotein catabolism links hypoglycemia to hypertriglyceridemia in Glycogen Storage Disease type Ia

Hoogerland

Peeks

Hijmans

et al. 2021

J of Inher Metab Disea

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Prevention of hypertriglyceridemia is one of the biomedical targets in Glycogen Storage Disease type Ia (GSD Ia) patients, yet it is unclear how hypoglycemia links to plasma triglyceride (TG) levels. We analyzed whole-body TG metabolism in normoglycemic (fed) and hypoglycemic (fasted) hepatocyte-specific glucose-6-phosphatase deficient (L-G6pc −/− ) mice. De novo fatty acid synthesis contributed substantially to hepatic TG accumulation in normoglycemic L-G6pc −/− mice. In hypoglycemic conditions, enhanced adipose tissue lipolysis was the main driver of liver steatosis, supported by elevated free fatty acid concentrations in GSD Ia mice and GSD Ia patients. Plasma very-low-density lipoprotein (VLDL) levels were increased in GSD Ia patients and in normoglycemic L-G6pc −/− mice, and further elevated in hypoglycemic L-G6pc −/− mice. VLDL-TG secretion rates were doubled in normo-and hypoglycemic L-G6pc −/− mice, while VLDL-TG catabolism was selectively inhibited in hypoglycemic L-G6pc −/− mice. In conclusion, fasting-induced hypoglycemia in

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Impaired Very‐Low‐Density Lipoprotein catabolism links hypoglycemia to hypertriglyceridemia in Glycogen Storage Disease type Ia

Hoogerland

Peeks

Hijmans

et al. 2021

J of Inher Metab Disea

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show abstract

“…More than any other cell type in the body, cells in the fat depot are confronted with extreme levels of free fatty acids, cholesterol and the effects of lipotoxicity [58]. To give an inkling of the challenges faced in the fat depot, in blood, the levels of free fatty acids range in the area from 0.2 to 0.4 mM and even a small increase in these levels is associated with a reduction in insulin release by the β-cell and a marked loss of insulin sensitivity in muscle [59–61].…”

Section: Living In the Fat Lanementioning

confidence: 99%

Guardian of corpulence: a hypothesis on p53 signaling in the fat cell

Bazuine¹,

Stenkula²,

Maggie³

et al. 2009

Clinical Lipidology

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Adipocytes provide an organism with fuel in times of caloric deficit, and are an important type of endocrine cell in the maintenance of metabolic homeostasis. In addition, as a lipid-sink, adipocytes serve an equally important role in the protection of organs from the damaging effects of ectopic lipid deposition. For the organism, it is of vital importance to maintain adipocyte viability, yet the fat depot is a demanding extracellular environment with high levels of interstitial free fatty acids and associated lipotoxic effects. These surroundings are less than beneficial for the overall health of any resident cell, adipocyte and preadipocyte alike. In this review, we discuss the process of adipogenesis and the potential involvement of the p53 tumor-suppressor protein in alleviating some of the cellular stress experienced by these cells. In particular, we discuss p53-mediated mechanisms that prevent damage caused by reactive oxygen species and the effects of lipotoxicity. We also suggest the potential for two p53 target genes, START domain-containing protein 4 (StARD4) and oxysterol-binding protein (OSBP), with the concomitant synthesis of the signaling molecule oxysterol, to participate in adipogenesis.

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“…RNA integrity was verified by means of 2% agarose gels. Messenger RNA was measured by Northern blot hybridization as described previously (51,52,54,56,88).…”

Section: Rat Preadipocyte Culturesmentioning

confidence: 99%

Fat depot origin affects fatty acid handling in cultured rat and human preadipocytes

Caserta¹,

Tchkonia²,

Civelek³

et al. 2001

American Journal of Physiology-Endocrinology and Metabolism

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Regional differences in free fatty acid (FFA) handling contribute to diseases associated with particular fat distributions. As cultured rat preadipocytes became differentiated, FFA transfer into preadipocytes increased and was more rapid in single perirenal than in epididymal cells matched for lipid content. Uptake by human omental preadipocytes was greater than uptake by abdominal subcutaneous preadipocytes. Adipose-specific fatty acid binding protein (aP2) and keratinocyte lipid binding protein abundance was higher in differentiated rat perirenal than in epididymal preadipocytes. This interdepot difference in preadipocyte aP2 expression was reflected in fat tissue in older animals. Carnitine palmitoyltransferase 1 activity increased during differentiation and was higher in perirenal than in epididymal preadipocytes, particularly the muscle isoform. Long-chain acyl-CoA levels were higher in perirenal than in epididymal preadipocytes and isolated fat cells. These data are consistent with interdepot differences in fatty acid flux ensuing from differences in fatty acid binding proteins and enzymes of fat metabolism. Heterogeneity among depots results, in part, from distinct intrinsic characteristics of adipose cells. Different depots are effectively separate miniorgans.

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Long-chain fatty acids decrease lipoprotein lipase activity of cultured rat adipocyte precursors

Cited by 11 publications

References 46 publications

Impaired Very‐Low‐Density Lipoprotein catabolism links hypoglycemia to hypertriglyceridemia in Glycogen Storage Disease type Ia

Impaired Very‐Low‐Density Lipoprotein catabolism links hypoglycemia to hypertriglyceridemia in Glycogen Storage Disease type Ia

Guardian of corpulence: a hypothesis on p53 signaling in the fat cell

Fat depot origin affects fatty acid handling in cultured rat and human preadipocytes

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