Stimulation of phosphatidylcholine synthesis by insulin and ATP in isolated rat adipocyte plasma membranes

Kiechle, Frederick L.; Malinski, Halina; Strandbergh, Donald R.; Artiss, Joseph D.

doi:10.1016/0006-291x(86)91167-8

Cited by 6 publications

(2 citation statements)

References 16 publications

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“…As discussed above, insulin increased the rate of PC synthesis via the de novo pathway by at least 60-fold. In addition to the de novo pathway, insulin also activates phospholipid methyltransferase (Kiechle et al, 1986) and CDP:phosphocholine cytidylyltransferase (Kelly et al, 1988), which stimulate PC synthesis from PE and DAG, respectively. These enzyme activations may contribute to PC synthesis, but the importance of the de novo PA synthesis pathway seems clear from the finding that inhibition of this pathway by pertussis toxin largely prevented PC resynthesis during insulin action.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of pertussis toxin on insulin-stimulated phosphatidylcholine hydrolysis and glycerolipid synthesis de novo. Studies in BC3H-1 myocytes and rat adipocytes

Hoffman¹,

Standaert²,

Nair³

et al. 1991

Biochemistry

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Insulin-induced increases in diacylglycerol (DAG) have been suggested to result from stimulation of de novo phosphatidic acid (PA) synthesis and phosphatidylcholine (PC) hydrolysis. Presently, we found that insulin decreased PC levels of BC3H-1 myocytes and rat adipocytes by approximately 10-25% within 30 s. These decreases were rapidly reversed in both cell types, apparently because of increased PC synthesis de novo. In BC3H-1 myocytes, pertussis toxin inhibited PC resynthesis and insulin effects on the pathway of de novo PA-DAG-PC synthesis, as evidenced by changes in [3H]glycerol incorporation, but did not inhibit insulin-stimulated PC hydrolysis. Pertussis toxin also blocked the later, but not the initial, increase in DAG production in the myocytes. Phorbol esters activated PC hydrolysis in both myocytes and adipocytes, but insulin-induced stimulation of PC hydrolysis was not dependent upon activation of PKC, since this hydrolysis was not inhibited by 500 microM sangivamycin, an effective PKC inhibitor. Our results indicate that insulin increases DAG by pertussis toxin sensitive (PA synthesis de novo) and insensitive (PC hydrolysis) mechanisms, which are mechanistically separate, but functionally interdependent and integrated. PC hydrolysis may contribute importantly to initial increases in DAG, but later sustained increases are apparently largely dependent on insulin-induced stimulation of the pathway of de novo phospholipid synthesis.

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Section: Discussionmentioning

confidence: 99%

Differential effects of pertussis toxin on insulin-stimulated phosphatidylcholine hydrolysis and glycerolipid synthesis de novo. Studies in BC3H-1 myocytes and rat adipocytes

Hoffman¹,

Standaert²,

Nair³

et al. 1991

Biochemistry

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“…The lower expression of PEMT we found in VAT and the lower accumulation of lipid droplets in PEMT-deficient adipocytes are also in agreement with the findings of several groups that reported a (somewhat counterintuitive) lower adipocyte size in VAT ( 32 , 33 ) and its association with insulin resistance ( 34 ). Further studies demonstrate that PEMT expression is regulated by insulin ( 35 , 36 ), and that ceramides induce insulin resistance ( 37–39 ). Taken together with these studies, our network-based analysis and our stem cell model suggest that PEMT forms a major metabolic junction that bridges a few biosynthetic pathways into a functional pathway in adipose tissues.…”

Section: Discussionmentioning

confidence: 99%

Distinct infrastructure of lipid networks in visceral and subcutaneous adipose tissues in overweight humans

Zacharia

Saidemberg

Mannully

et al. 2020

The American Journal of Clinical Nutrition

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Background Adipose tissue plays important roles in health and disease. Given the unique association of visceral adipose tissue with obesity-related metabolic diseases, the distribution of lipids between the major fat depots located in subcutaneous and visceral regions may shed new light on adipose tissue–specific roles in systemic metabolic perturbations. Objective We sought to characterize the lipid networks and unveil differences in the metabolic infrastructure of the 2 adipose tissues that may have functional and nutritional implications. Methods Paired visceral and subcutaneous adipose tissue samples were obtained from 17 overweight patients undergoing elective abdominal surgery. Ultra-performance LC-MS was used to measure 18,640 adipose-derived features; 520 were putatively identified. A stem cell model for adipogenesis was used to study the functional implications of the differences found. Results Our analyses resulted in detailed lipid metabolic maps of the 2 major adipose tissues. They point to a higher accumulation of phosphatidylcholines, triacylglycerols, and diacylglycerols, although lower ceramide concentrations, in subcutaneous tissue. The degree of unsaturation was lower in visceral adipose tissue (VAT) phospholipids, indicating lower unsaturated fatty acid incorporation into adipose tissue. The differential abundance of phosphatidylcholines we found can be attributed at least partially to higher expression of phosphatidylethanolamine methyl transferase (PEMT). PEMT-deficient embryonic stem cells showed a dramatic decrease in adipogenesis, and the resulting adipocytes exhibited lower accumulation of lipid droplets, in line with the lower concentrations of glycerolipids in VAT. Ceramides may inhibit the expression of PEMT by increased insulin resistance, thus potentially suggesting a functional pathway that integrates ceramide, PEMT, and glycerolipid biosynthetic pathways. Conclusions Our work unveils differential infrastructure of the lipid networks in visceral and subcutaneous adipose tissues and suggests an integrative pathway, with a discriminative flux between adipose tissues.

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Fluorometric determination of phosphatidylcholine as a measure of phospholipid methylation

Dandurand

Kiechle

Strandbergh

et al. 1991

Analytical Biochemistry

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Stimulation of phosphatidylcholine synthesis by insulin and ATP in isolated rat adipocyte plasma membranes

Cited by 6 publications

References 16 publications

Differential effects of pertussis toxin on insulin-stimulated phosphatidylcholine hydrolysis and glycerolipid synthesis de novo. Studies in BC3H-1 myocytes and rat adipocytes

Differential effects of pertussis toxin on insulin-stimulated phosphatidylcholine hydrolysis and glycerolipid synthesis de novo. Studies in BC3H-1 myocytes and rat adipocytes

Distinct infrastructure of lipid networks in visceral and subcutaneous adipose tissues in overweight humans

Fluorometric determination of phosphatidylcholine as a measure of phospholipid methylation

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