Serum fatty acid profiles in type I and type II diabetes: Metabolic alterations of fatty acids of the main serum lipids

Seigneur, M.; Freyburger, G.; Gin, H.; Claverie, M.; Lardeau, D.; Lacape, G.; Moigne, F. Le; Crockett, R; Boisseau, M. R.

doi:10.1016/0168-8227(94)90101-5

Cited by 44 publications

(34 citation statements)

References 18 publications

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“…Sphingomyelins are generated by virtue of both salvage and de novo ceramide pathways (37), which may be relevant to their debated role in health and disease. Epidemiologic data demonstrate a positive correlation between total serum sphingomyelin concentration and CVD (18,29), yet total serum sphingomyelin has been reported as lower in CVD-prone states such as obesity, type 1 diabetes, and type 2 diabetes (35,39). Metabolomic profiling has helped clarify this discrepancy by associating certain sphingomyelin species, rather than total concentration, with metabolic parameters.…”

Section: Discussionmentioning

confidence: 99%

Serum sphingolipids: relationships to insulin sensitivity and changes with exercise in humans

Bergman

Brozinick

Strauss

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

123

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Ceramides and sphingolipids are a family of lipid molecules that circulate in serum and accumulate in skeletal muscle, promoting insulin resistance. Plasma ceramide and dihydroceramide are related to insulin resistance, yet less is known regarding other ceramide and sphingolipid species. Despite its association with insulin sensitivity, chronic endurance exercise training does not change plasma ceramide and sphingolipid content, with little known regarding a single bout of exercise. We measured basal relationships and the effect of acute exercise (1.5 h at 50% V O2 max) and recovery on serum ceramide and sphingolipid content in sedentary obese individuals, endurancetrained athletes, and individuals with type 2 diabetes (T2D). Basal serum C18:0, C20:0, and C24:1 ceramide and C18:0 and total dihydroceramide were significantly higher in T2D and, along with C16:0 ceramide and C18:0 sphingomyelin, correlated positively with insulin resistance. Acute exercise significantly increased serum ceramide, glucosylceramide, and GM3 gangliosides, which largely decreased to basal values in recovery. Sphingosine 1-phosphate and sphingomyelin did not change during exercise but decreased below basal values in recovery. Serum C16:0 and C18:0 ceramide and C18:0 sphingomyelin, but not the total concentrations of either of them, were positively correlated with markers of muscle NF-B activation, suggesting that specific species activate intracellular inflammation. Interestingly, a subset of sphingomyelin species, notably C14:0, C22:3, and C24:4 species, was positively associated with insulin secretion and glucose tolerance. Together, these data show that unique ceramide and sphingolipid species associate with either protective or deleterious features for diabetes and could provide novel therapeutic targets for the future. insulin sensitivity; athlete's paradox; lipid composition; plasma biomarkers THE GLOBAL BURDEN OF DIABETES continues to rise, fueled by the even greater epidemic of prediabetes (9). Nevertheless, not all of those with prediabetes will develop diabetes (27), highlighting the need to identify nonglycemic markers of disease progression that may also prove useful as new targets for the treatment of diabetes itself. Advances in lipidomics have provided new tools to investigate processes that govern the development of diabetes and its complications beyond that of glucose itself. Serum ceramides, a family of sphingolipids involved in diverse and relevant metabolic processes, have received considerable attention in relation to diabetes, making them prime candidates for further examination. Unlike other biomarkers, discrete serum ceramide profiles are rendered across the spectrum of diabetogenesis, creating speculation that ceramides not only mark but contribute to the disease process (8, 17).Much of this speculation is derived from data generated from in vitro and animal experimentation. Human data to date are limited largely to associations between serum ceramide concentration and risk for both diabetes (15) and related comp...

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Section: Discussionmentioning

confidence: 99%

Serum sphingolipids: relationships to insulin sensitivity and changes with exercise in humans

Bergman

Brozinick

Strauss

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

123

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“…Fatty acids are known to be important biomedical indicators of the abnormal lipid metabolism in diabetes mellitus and extensive studies have been undertaken to investigate the changes of fatty acid profiles in diabetic patients [15][16][17][18][19][20][21]. In several studies it has been shown that the fatty acid composition of serum lipids [22] and of skeletal muscle phospholipids [22,23] influence insulin sensitivity.…”

Section: Introductionmentioning

confidence: 99%

Discrimination of Type 2 diabetic patients from healthy controls by using metabonomics method based on their serum fatty acid profiles

Yang

Hong

et al. 2004

Journal of Chromatography B

107

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“…This study shows that OA, one of the most common fatty acids in triglycerides in people and animals with and without diabetes [17,19,20], strongly enhances the mitogenic effects of PDGF-BB in primary human SMCs. Previous studies have shown that OA also enhances the growth-promoting activity of angiotensin II [50], endothelin-1 [51], and IGF-I [52] in SMCs derived from other species.…”

Section: Oa Could Mediate Its Mitogenic Effects By Causing Increased mentioning

confidence: 99%

“…Although relative levels of oleate (expressed as percentage of total fatty acids) in circulating triglycerides are often found to be similar in people and animals with and without Type 1 diabetes [17,20], some studies have shown an increased level of oleate in triglycerides or total serum lipids from Type 2 diabetic patients compared to non-diabetic patients [20,61]. Furthermore, circulating levels of free fatty acids, including oleate, have been reported to be increased in subjects with Type 2 diabetes [15,62,63].…”

Section: Increased Levels Of Circulating Oa-containing Triglycerides mentioning

confidence: 99%

“…NEFAs are liberated from triglycerides in the arterial wall by lipoprotein lipase [18]. The main fatty acids present in triglycerides in humans with and without diabetes are oleate and palmitate [19,20]. Increased levels of circulating triglycerides in combination with hydrolysis of these triglycerides in the atherosclerotic plaque are likely to result in increased levels of NEFAs within the plaque.…”

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confidence: 99%

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Oleate, not ligands of the receptor for advanced glycation end-products, promotes proliferation of human arterial smooth muscle cells

et al. 2003

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Aims/hypothesis. Diabetes accelerates cardiovascular disease caused by atherosclerosis. Accordingly, diabetes accelerates atherosclerotic lesion progression and increases arterial smooth muscle cell proliferation. We hypothesized that diabetes can exert growth-promoting effects on smooth muscle cells via increased advanced glycation end-products or by dyslipidaemia. Methods. Primary human arterial smooth muscle cells were stimulated with advanced glycation end-products, other ligands of the receptor for advanced glycation end-products or fatty acids common in triglycerides. Cell proliferation was measured as DNA synthesis, cell cycle distribution and cell number. Effects of oleate on cellular phospholipids, diacylglycerol, triglycerides and cholesterol esters were analyzed by thin-layer chromatography, and oleate accumulation into diacylglycerol was confirmed by gas chromatography. Results. Human arterial smooth muscle cells express the receptor for advanced glycation end-products, but its ligands N ε -(carboxymethyl)lysine-modified proteins, methylglyoxal-modified proteins, S100B polypeptide and amyloid-β (1-40) peptide, exert no mitogenic action. Instead, oleate, one of the most common fatty acids in triglycerides, enhances platelet-derived growth factor-BB-mediated proliferation and oleate-containing 1,2-diacylglycerol formation in smooth muscle cells. This mitogenic effect of oleate depends on phospholipase D activity and is associated with an increased formation of oleate-enriched 1,2-diacylglycerol. Conclusion/interpretation. Oleate, not ligands of the receptor for advanced glycation end-products, acts as an enhancer of human smooth muscle cell proliferation. Thus, lipid abnormalities, rather than hyperglycaemia, could be a major factor promoting proliferation of smooth muscle cells in atherosclerotic lesions. [Diabetologia (2003[Diabetologia ( ) 46:1676[Diabetologia ( -1687 Keywords Atherosclerosis, diabetes, diacylglycerol, fatty acids, platelet-derived growth factor, phospholipase D, triglycerides. Atherosclerosis is accelerated by both Type I and Type 2 diabetes [1] by mechanisms that are poorly understood. Proliferation of arterial smooth muscle cells (SMCs) in lesions of atherosclerosis plays an important role in progression of early fatty streaks to fibroatheromas. We have recently reported that increased SMC proliferation in fibroatheromas occurs concomitantly with hyperglycaemia and an increased plasma triglyceride concentration in a porcine model of diabetes-accelerated atherosclerosis [2]. However, increased plasma glucose concentrations do not directly stimulate proliferation of SMCs isolated from these animals or from human subjects [2]. In this study, we investigated advanced glycation end-products (AGEs)

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Serum fatty acid profiles in type I and type II diabetes: Metabolic alterations of fatty acids of the main serum lipids

Cited by 44 publications

References 18 publications

Serum sphingolipids: relationships to insulin sensitivity and changes with exercise in humans

Serum sphingolipids: relationships to insulin sensitivity and changes with exercise in humans

Discrimination of Type 2 diabetic patients from healthy controls by using metabonomics method based on their serum fatty acid profiles

Oleate, not ligands of the receptor for advanced glycation end-products, promotes proliferation of human arterial smooth muscle cells

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