Effects of fenofibrate and insulin on the biosynthesis of unsaturated fatty acids in streptozotocin diabetic rats

2005 ◽  
Vol 73 (5) ◽  
pp. 369-378 ◽  
Author(s):  
Mauro A. Montanaro ◽  
Ana M. Bernasconi ◽  
Marìa S. González ◽  
Omar J. Rimoldi ◽  
Rodolfo R. Brenner
1985 ◽  
Vol 230 (2) ◽  
pp. 329-337 ◽  
Author(s):  
H Osmundsen ◽  
K Bjørnstad

Evidence showing that some unsaturated fatty acids, and in particular docosahexaenoic acid, can be powerful inhibitors of mitochondrial β-oxidation is presented. This inhibitory property is, however, also observed with the cis- and trans-isomers of the C18:1(16) acid. Hence it is probably the position of the double bond(s), and not the degree of unsaturation, which confers the inhibitory property. It is suggested that the inhibitory effect is caused by accumulation of 2,4-di- or 2,4,7-tri-enoyl-CoA esters in the mitochondrial matrix. This has previously been shown to occur with these fatty acids, in particular when the supply of NADPH was limiting 2,4-dienoyl-CoA reductase (EC 1.3.1.-) activity [Hiltunen, Osmundsen & Bremer (1983) Biochim. Biophys. Acta 752, 223-232]. Liver mitochondria from streptozotocin-diabetic rats showed an increased ability to β-oxidize 2,4-dienoyl-CoA-requiring acylcarnitines. Docosahexaenoylcarnitine was also found to be less inhibitory at lower concentrations with incubation under coupled conditions. With uncoupling conditions there was little difference between mitochondria from normal and diabetic rats in these respects. This correlates with a 5-fold stimulation of 2,4-dienoyl-CoA reductase activity found in mitochondria from streptozotocin-diabetic rats.


2014 ◽  
Vol 53 (2) ◽  
pp. 237-246 ◽  
Author(s):  
Melisa Kurtz ◽  
Evangelina Capobianco ◽  
Nora Martinez ◽  
Sabrina Lorena Roberti ◽  
Edith Arany ◽  
...  

In maternal diabetes, the fetal heart can be structurally and functionally affected. Maternal diets enriched in certain unsaturated fatty acids can activate the nuclear receptors peroxisome proliferator-activated receptors (PPARs) and regulate metabolic and anti-inflammatory pathways during development. Our aim was to investigate whether PPARα expression, lipid metabolism, lipoperoxidation, and nitric oxide (NO) production are altered in the fetal hearts of diabetic rats, and to analyze the putative effects ofin vivoPPAR activation on these parameters. We found decreased PPARα expression in the hearts of male but not female fetuses of diabetic rats when compared with controls. Fetal treatments with the PPARα ligand leukotriene B4upregulated the expression of PPARα and target genes involved in fatty acid oxidation in the fetal hearts. Increased concentrations of triglycerides, cholesterol, and phospholipids were found in the hearts of fetuses of diabetic rats. Maternal treatments with diets supplemented with 6% olive oil or 6% safflower oil, enriched in unsaturated fatty acids that can activate PPARs, led to few changes in lipid concentrations, but up-regulated PPARα expression in fetal hearts. NO production, which was increased in the hearts of male and female fetuses in the diabetic group, and lipoperoxidation, which was increased in the hearts of male fetuses in the diabetic group, was reduced by the maternal treatments supplemented with safflower oil. In conclusion, impaired PPARα expression, altered lipid metabolism, and increased oxidative and nitridergic pathways were evidenced in hearts of fetuses of diabetic rats and were regulated in a gender-dependent manner by treatments enriched with PPAR ligands.


2017 ◽  
Vol 5 (1) ◽  
pp. 22-28
Author(s):  
Nazi Aghaalikhani ◽  
Mohammad Taghi Goodarzi ◽  
Zeinab Latifi ◽  
Azam Rezaei Farimani ◽  
Amir Fattahi

Background: Several studies have shown association of fatty acids with type 2 diabetes (T2D), as well as metformin effects on blood glucose concentrations through affecting lipid metabolism. Objectives: Since the exact therapeutic mechanism of metformin is not clear, in this study we investigated effects of different doses of metformin on serum fatty acids in rats with T2D. Materials and Methods: Twenty-five adult albino male Wistar rats were divided into the following groups: Healthy, untreated T2D, and T2D rats receiving metformin for 4 weeks with doses of 100, 150, and 200 mg/kg/d. Serum insulin and triglyceride (TG) were measured using commercial kits. Serum total lipids were extracted by the Bligh-Dyer method and then compositions of fatty acids were evaluated using gas chromatograph. Results: Monounsaturated fatty acid (MUFA) levels in T2D rats were lower than those in healthy rats (P < 0.05). We also observed that diabetic rats treated with 100 or 150 mg/kg/d of metformin had higher levels of arachidonic acid and polyunsaturated fatty acids (PUFA) in comparison with the healthy group (P < 0.05). Moreover, the T2D+Met (150 mg/kg) group showed increased levels of MUFA compared with the T2D group. Such a difference was seen in levels of arachidonic acid between the T2D+Met 100 mg/ kg group and untreated T2D group. In the group treated with high doses of metformin (200 mg/kg/d), levels of palmitic acid, palmitoleic acid, and saturated fatty acid (SFA) were higher and levels of oleic acid, linoleic acid, arachidonic acid, MUFA, PUFA, and also SFA/UFA ratio were lower compared with other metformin treated and untreated groups (P < .05). In untreated T2D group, there were positive correlations between glucose levels and linoleic acid and PUFA levels (r = 0.707, P = .049 and r = 0.726, P = .041 respectively). Arachidonic acid levels were positively correlated with glucose levels in T2D rats treated with 100 mg/kg/d of metformin (r = 0.969, P = .031). Conclusions: Our study showed that different doses of metformin could have different effects on serum levels of saturated and unsaturated fatty acids, as 200 mg/kg/d of metformin could increase and decrease saturated and unsaturated fatty acids respectively, while lower doses increased unsaturated fatty acids, particularly arachidonic acid.


1990 ◽  
Vol 68 (9) ◽  
pp. 1177-1182 ◽  
Author(s):  
Terje S. Larsen ◽  
David L. Severson

The effect of oleate (0.3 and 1.2 mM) and the combined effect of β-hydroxybutyrate (4 and 8 mM) and acetoacetate (1 and 2 mM) on rates of lipolysis (glycerol output) was determined with calcium-tolerant myocytes isolated from the hearts of normal rats and hearts from acutely (2–3 days; 100 mg/kg streptozotocin) diabetic rats. In addition, the effect of these exogenous substrates on rates of lipolysis was investigated in triacylglycerol (TG) loaded myocytes prepared from normal hearts by inclusion of oleate in the isolation solutions. Diabetic and TG-loaded myocytes had higher lipolytic rates than normal myocytes. In control myocytes, oleate (1.2 mM) did not affect basal lipolysis, but it reduced isoproterenol-stimulated lipolysis by 30%. In diabetic and TG-loaded myocytes, the addition of 1.2 mM oleate inhibited basal rates of lipolysis by 41 and 40%, respectively, and isoproterenol-stimulated rates of lipolysis by 43 and 53%, respectively. However, lipolytic rates measured in the presence of 1.2 mM oleate with diabetic and TG-loaded myocytes were still higher than lipolysis in normal myocytes incubated in the absence of oleate. Ketone bodies increased both basal and isoproterenol-stimulated lipolysis in normal myocytes. In diabetic myocytes, ketone bodies produced a modest stimulation of basal lipolysis but had no effect on isoproterenol-stimulated rates of lipolysis. These data indicate that mobilization of endogenous TG may play an important role in supplying energy to the heart in the diabetic state. Moreover, accumulation of endogenous TG in diabetic myocardium can only partly be explained by inhibition of lipolysis by exogenous substrates.Key words: lipolysis, cardiac myocytes, diabetes.


Author(s):  
Abdulrahman L. Al-Malki ◽  
Elie K. Barbour ◽  
Khadijah S. Balamash ◽  
Fawzia A. Alshubaily ◽  
Khalid O. Abualnaja ◽  
...  

Aim: This study evaluated the effect of Phyocyanin extracted from Chlorophyta Ulva lactuca algae loaded on albumin nano-particles (ULANP) on diabetic rats. Materials and Methods: Fifty albino rats were divided into 5 goups.  GPI: control and GPII: rats were injected with alloxan (75 mg /kg) i.p for six consecutive days for induction of diabetes. This group was subdivided into 4 subgroups: GP IIa: (Untreated diabetic): GP IIb: rats were given with ULANP (100 mg/kg).GP IIc: Rats were given ULANP (200 mg/kg) i.p. GP IId: Rats were given insulin (100 unit/ day). Serum NO, interleukin-6 glucose, AGEs and fatty acids profile was determined. Results:  Analysis of ULANP by FTIR showed the characteristic band (2100 cm-1~ 3700 cm-1) that is indicated mainly from -COO, – CO and conjugated double bond. These bonds showed spectral bands peak 2985 cm-1 and 2860 cm-1, 2986 cm-1.  Administration of ULANP in diabetic rats exerted an anti-inflammatory by lowering NO and IL-6 levels and hypoglycemic effects by decreased glucose and reduced AGEs levels. In addition, ULAPN lowered percent of saturated fatty acids while elevated unsaturated fatty acids percent. Conclusion: It was concluded that, ULAPN is a promising effective anti-inflammatory and hypoglycemic agent compared with other therapeutic agents with lower site effects. 


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