[1] Citrate synthase

Srere, Paul A.

doi:10.1016/0076-6879(69)13005-0

Cited by 2,097 publications

(1,063 citation statements)

References 24 publications

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“…The activity was expressed as a first-order rate constant, k, per min. Citrate synthase activity was also measured in cell lysates obtained by lauryl maltoside treatment, essentially as described by Srere (1969). Hybridisation signals with [ 32 P]-labelled probes were measured using a PhosphorImager™ (Molecular Dynamics, Sunnyvale, Calif., USA).…”

Section: Methodsmentioning

confidence: 99%

Preferential amplification and phenotypic selection in a population of deleted and wild-type mitochondrial DNA in cultured cells

et al. 1997

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Section: Methodsmentioning

confidence: 99%

Preferential amplification and phenotypic selection in a population of deleted and wild-type mitochondrial DNA in cultured cells

et al. 1997

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“…Muscle (5-10 mg) was homogenized in 1:50 dilution (w/v) of a 175 mmol/l potassium buffer solution and citrate synthase activity was assayed spectrophotometrically at 25°C as previously described [16]. β-HAD activity was assayed spectrophotometrically at 25°C measuring the disappearance of NADH using the same homogenate as for citrate synthase [17].…”

Section: Intramuscular Triglyceride Concentrationmentioning

confidence: 99%

Disassociation of muscle triglyceride content and insulin sensitivity after exercise training in patients with Type 2 diabetes

et al. 2004

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Aim/hypothesis. We determined the effect of exercise training on insulin sensitivity and muscle lipids (triglyceride [TG m ] and long-chain fatty acyl CoA [LCACoA] concentration) in patients with Type 2 diabetes. Methods. Seven patients with Type 2 diabetes and six healthy control subjects who were matched for age, BMI, % body fat and VO 2 peak participated in a 3 days per week training program for 8 weeks. Insulin sensitivity was determined pre-and post-training during a 120 min euglycaemic-hyperinsulinaemic clamp and muscle biopsies were obtained before and after each clamp. Oxidative enzyme activities [citrate synthase (CS), β-hydroxy-acyl-CoA (β-HAD)] and TG m were determined from basal muscle samples pre-and post training, while total LCACoA content was measured in samples obtained before and after insulinstimulation, pre-and post training. Results. The training-induced increase in VO 2 peak (~20%, p<0.01) was similar in both groups. Compared with control subjects, insulin sensitivity was lower in the diabetic patients before and after training (~60%; p<0.05), but was increased to the same extent in both groups with training (~30%; p<0.01). TG m was increased in patients with Type 2 diabetes (170%; p<0.05) before, but was normalized to levels observed in control subjects after training. Basal LCACoA content was similar between groups and was unaltered by training. Insulin-stimulation had no detectable effect on LCACoA content. CS and β-HAD activity were increased to the same extent in both groups in response to training (p<0.001). Conclusion/interpretation. We conclude that the enhanced insulin sensitivity observed after short-term exercise training was associated with a marked decrease in TG m content in patients with Type 2 diabetes. However, despite the normalization of TG m to levels observed in healthy individuals, insulin resistance was not completely reversed in the diabetic patients. Type 2 diabetes is characterized by skeletal muscle insulin resistance and impaired glucose metabolism. In addition to disturbances in glucose homeostasis, individuals with Type 2 diabetes have an impaired lipid metabolism, reflected by increased circulating free fatty acids [1], reduced rates of whole body fat oxidation [2] and excessive deposition of lipids in various tissues including skeletal muscle [3]. With regard to muscle lipid status, there is evidence in humans that increased trigacylglycerol (TG m ) concentration [3,4,5,6,7] and increased long-chain fatty acyl CoA (LCACoA) content are negatively associated with whole body insulin action [8]. Considering the rela-

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“…PEPCK activity was assayed in the cytosolic fraction according to the method of Chang and Lane [24]. Citrate synthase activity was measured by spectrophotometry in the presence of 5,5′-dithiobis-(2-nitro-benzoate) as previously described [25].…”

Section: Methodsmentioning

confidence: 99%

Acute and selective regulation of glyceroneogenesis and cytosolic phosphoenolpyruvate carboxykinase in adipose tissue by thiazolidinediones in type 2 diabetes

et al. 2007

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[1] Citrate synthase

Cited by 2,097 publications

References 24 publications

Preferential amplification and phenotypic selection in a population of deleted and wild-type mitochondrial DNA in cultured cells

Preferential amplification and phenotypic selection in a population of deleted and wild-type mitochondrial DNA in cultured cells

Disassociation of muscle triglyceride content and insulin sensitivity after exercise training in patients with Type 2 diabetes

Acute and selective regulation of glyceroneogenesis and cytosolic phosphoenolpyruvate carboxykinase in adipose tissue by thiazolidinediones in type 2 diabetes

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