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OBJECTIVE: To observe the effect of electroacupuncture(EA) at "Shenmen"(HT7) and "Sanyinjiao"(SP6)on energy metabolism in paraventricular nucleus (PVN) of hypothalamus in insomnia rats, so as to explore its mechanism underlying improvement of insomnia. METHODS: A total of 66 SD rats (half male and half female) were randomized into 3 groups：normal control, model and EA groups(n＝22 per group). The insomnia model was established by binding the rat for at least 4 h (step increase of 30 min per day), once daily for 15 days. EA (5 Hz /25 Hz, 0.5－1.0 mA) was applied to unilateral HT7 and SP6 for 15 min, once daily for 5 days. The rats' spontaneous activities during day and night were recorded by using the ClockLab Data Collection and Analysis System, and the duration of exhausted swimming was detected by using load-bearing endurance swimming test. The expression of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) of PVN tissue was assayed by Western blot, and the contents of acetyl coenzyme A (Ac-CoA) and Na＋-K＋adenosine triphosphatase (Na＋-K＋-ATPase) in the PVN tissue, and corticosterone (CORT) in plasma were assayed by ELISA. Changes of the ultrastructure of PVN cells were observed by transmission electron microscope. RESULTS: After modeling, the rats' daytime and nocturnal locomotor activities were significantly increased and decreased, respectively (P<0.05), and the duration of exhausted swimming was considerably shortened in the model group compared with that of the normal control group (P<0.05). The expression level of AMPK protein in the PVN was obviously up-regulated (P<0.05), and the contents of Ac-CoA and Na＋-K＋-ATPase in PVN and CORT in plasma were markedly decreased in the model control group relevant to the normal group (P<0.05). After EA intervention, the increased daytime locomotion and the decreased nocturnal activities, the shortened duration of exhausted swimming, the up-regulated expression of AMPK, and the decreased Ac-CoA, Na＋-K＋-ATPase and CORT contents were all reversed in the EA treated rats relevant to those of the insomnia rats (all P<0.05). Moreover, ultrastructural observation showed mitochondrial swelling and disappearance of partial ribosomes in the plasma of PVN cells in the model group, while in the EA group, only mild swelling of some mitochondria was found, being with basically normal nuclear membrane, mitochondria, rough endoplasmic reticulum, Golgi complex and ribosomes. CONCLUSION: EA at HT7 and SP6 has a positive effect in improving insomnia and insomnia-induced fatigue in insomnia rats, which may be associated with its effects in restraining the expression of AMPK protein, and up-regulating the contents of Ac-CoA and Na＋-K＋-ATPase in PVN and CORT in plasma.
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Cardiovascular manifestations in a patient with congestive heart failure, which disappeared in short course of time, ignited the idea to think of unusuality from common rheumatic heart disease (RHD). Cardiac events that reversed within 2 days of admission in a chronic alcoholic, whose diagnosis puzzled us, are presented here. A retrospective conclusion of wet beri-beri is made, as all the haemodynamic sequelae vanished with thiamine replacement.
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Objective: To investigate the signal molecules and signal transduction involved in endophytic fungal elicitor-induced atractylodin biosynthesis and the effect of an endophytic fungal elicitor on the key enzyme activity in Atractylodes lancea. Methods: Content changes of nitric oxide (NO), salicylic acid (SA), and atractylodin were detected under the endophytic fungal elicitor treatment by plant cell suspension culture technology. Results: The endophytic fungal elicitor remarkably promoted NO burst and the biosynthesis of SA and atractyodin by activating nitric oxide synthase (NOS), phenylalanine ammonia lyase (PAL), and acetyl coenzyme A carboxylase (ACC), respectively. NOS inhibitor PBITU could inhibit the NO and SA accumulation and the atractyodin biosynthesis induced by the elicitor. And atractyodin biosynthesis could also be triggered by exogenous NO or SA. The results indicated that NO and SA were the necessary signal molecules and NO burst was mediated by NOS induced by endophytic fungal elicitor. NO quencher cPITO could effectively remove NO burst in A. lancea cell induced by endophytic fungal elicitor and notably inhibit the biosynthesis promotion of SA and atractyodin in A. lancea cell induced by endophytic fungal elicitor. Exogenous SNP could reverse the cPITO inhibition on the activity of PAL and ACC and the synthesis of SA and atractylodin. This suggested that NO was an upstream signal molecule mediated endophytic fungal elicitor to accelerate the biosynthesis of SA and atractyodin. Conclusion: Endophytic fungal elicitor mediated through NO followed by SA could promote atractyodin biosynthesis by activating ACC in A. lancea.
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Objective To investigate the effects of high-fat diet on fatty acid metabolism, expression and activity of acetyl coenzyme A carboxylase (ACC) in skeletal muscle in rats. Methods Male Wistar rats aged 22-24 months were randomly divided into old control (OC) group and high-fat diet (HF) group. Male Wistar rats aged 4-5 months were selected as young control (YC) group. The rats in OC and YC groups were fed with basic diet, and the rats in HF group received high-fat diet. Insulin sensitivity was evaluated by hyperinsulinemic-euglycemic clamp technique. Skeletal muscle triglyceride was extracted and measured by an automated biochemistry analyzer. Long-chain acetyl coenzyme A (LCACoAs) were extracted from muscle and measured by a fluorospectrophotometer. Protein expressions of ACC and P-ACC were measured using SDS-PAGE and Western blot techniques. Results (1)Fasting blood glucose (FBG), fasting insulin (FINS) and free fatty acid were higher in OC group than in YC group and they increased significantly in HF group. Triglyceride (TG) and total cholesterol (TO levels were also elevated after high-fat feeding. (2)Glucose infusion rates (GIR) were reduced in OC group than in YC group, and decreased significantly after high-fat feeding. GIR was lower at the end of the 8th week than at the end of the 4th week in HF group. (3) Compared with YC group, skeletal muscle triglyceride and LCACoAs increased in OC group and increased significantly in HF group. (4)No alterations of protein levels of ACC in skeletal muscle were detected among three groups (P>0.05). The protein levels of P-ACC in skeletal muscle were lower in OC group, and much lower in HF group than in YC group (P<0.05 or P<0.01). Conclusions Compared with young rats, abnormal fatty acid metabolism and insulin resistance always exist in aged rats. High-fat feeding results in a significant increase in lipid content in skeletal muscle. Alterations of ACC activity may contribute to fat accumulation in skeletal muscle and insulin resistance.
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Rat liver lipoyl transacetylase catalyzes the formation of acetyl dihydrolipoic acid from acetyl coenzyme A and dihydrolipoic acid. In an earlier paper the formation of acetyl dihydrolipoic from pyruvate and dihydrolipoic acid catalyzed by pyruvate dehydrogenase has been reported. Acetyl dihydrolipoic acid is a substrate for citrate synthase, acetyl coenzyme A carboxylase and fatty acid synthetase. The Vmax. for citrate synthase with acetyl dihydrolipoic acid was identical to acetyl coenzyme A (approximately 1 μmol citrate formed/min/mg protein) while the apparent Km was approximately 4 times higher with acetyl dihydrolipoic acid as the substrate. This may be due to the fact that synthetic acetyl dihydrolipoic acid is a mixture of 4 possible isomers and only one of them may be the substrate for the enzymatic reaction. While dihydrolipoic acid can replace coenzyme A in the activation of succinate catalyzed by succinyl coenzyme A synthetase, the transfer of coenzyme A between succinate and acetoacetyl dihydrolipoic acid catalyzed by succinyl coenzyme A: 3 oxo-acid coenzyme A transferase does not occur.
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Intraperitoneal administration of lipoic acid (10 mg/100 g) does not effect changes in serum insulin levels in normal and alloxan diabetic rats, while normalising increased serum pyruvate, and impaired liver pyruvic dehydrogenase characteristic of the diabetic state. Dihydrolipoic acid has been shown to participate in activation of fatty acids with equal facility as coenzyme A. Fatty acyl dihydrolipoic acid however is sparsely thiolyzed to yield acetyl dihydrolipoic acid. Also acetyl dihydrolipoic acid does not activate pyruvate carboxylase unlike acetyl coenzyme A. The reduced thiolysis of ß-keto fatty acyl dihydrolipoic acid esters and the lack of activation of pyruvic carboxylase by acetyl dihydrolipoic acid could account for the antiketotic and antigluconeogenic effects of lipoic acid.