Request For Studies/research

[EL GAUCHO]

Hey bros,
I'm doing some research on a supplement containing the following ingredients:
Citrulline Malate
Citruline Ethyl-Ester HCL
Beta Alanine
L-Hystidine
Nicotinic Acid

Any studies/research/tests on the above would be appreciated.
If anyone has these saved or access to them, please post them as I would also like to read them....or at least their conclusions!
Thanks in advance.

EG.

 

[EL GAUCHO]

Plenty Of Karma Available!!!

 

[AX_Ryan]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed

http://www.ncbi.nlm.nih.gov/entrez/...d&dopt=Abstract&list_uids=16223757&query_hl=3

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed

http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/nia_0184.shtml

 

[AX_Ryan]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3112294&dopt=Abstract

Citruline Malate
Bendahan D, Mattei JP, Ghattas B, et al. 2002. Citrulline/malate promotes aerobic energy production in human exercising muscle. Br J Sports Med; 36(4):282-9.

Briand J, Blehaut H, Calvayrac R, Laval-Martin D. 1992. Use of a microbial model for the determination of drug effects on cell metabolism and energetics: study of citrulline-malate. Biopharm Drug Dispos; 13(1):1-22.

Callis A, Magnan de Bornier B, Serrano JJ, et al. 1991.Activity of citrulline malate on acid-base balance and blood ammonia and amino acid levels. Study in the animal and in man. Arzneimittelforschung; 41(6):660-3.

Fornaris E, Vanuxem J, Duflot P, et al. 1984. [Pharmacological/clinical approach of citrulline malate activity: study of blood lactate levels during standardized muscular exercise]. Gazette Medicale, 91(11):125-128.

Goubel F, Vanhoutte C, Allaf O, et al. 1997. Citrulline malate limits increase in muscle fatigue induced by bacterial endotoxins. Can J Physiol Pharmacol; 75(3):205-7.

Hartman WJ, Torre PM, Prior RL. 1994. Dietary citrulline but not ornithine counteracts dietary arginine deficiency in rats by increasing splanchnic release of citrulline. J Nutr; 124(10):1950-60.

Janeira MA, Santos PJ. 1998. Citrulline malate effects on the aerobic-anaerobic threshold and in post-exercise blood lactate recovery. Med Sci Sports Exerc; 30(5 supp): abstract 881.

Vanuxem D, Duflot JC, Prevot H, et al. 1990. [Influence of an anti-astenia agent, citrulline malate, on serum lactate and ammonia kinetics during a maximum exercise test in sedentary subjects]. Sem Hop Paris; 66(9):477-481.

Waugh WH, Daeschner CW, Files BA, et al. 2001. Oral citrulline as arginine precursor may be beneficial in sickle cell disease: early phase, two results. J Natl Med Assoc; 93(10):363-71.

 

[Lifterforlife]

Nicotinic acid

http://www.ncbi.nlm.nih.gov/entrez/...d&dopt=Abstract&list_uids=16322797&query_hl=4

http://www.ncbi.nlm.nih.gov/entrez/...d&dopt=Abstract&list_uids=16311212&query_hl=4

Human fat cell lipolysis: Biochemistry, regulation and clinical role.

Arner P.

Department of Medicine M63, Karolinska Institutet, Karolinska University Hospital, Huddinge, SE-141 86 Stockholm, Sweden.

Release of fatty acids (FAs) from adipose tissue through lipolysis in fat cells is a key event in many processes. FAs are not only energy substrates but also signalling molecules and substrates for lipoprotein production by the liver. Fat cells consist of>95% triglycerides that are hydrolysed during lipolysis to glycerol and FAs. The major rate-limiting factor for lipolysis is hormone-sensitive lipase, but additional lipases such as adipose tissue triglyceride lipase may also play a role. The regulation of human fat cell lipolysis is, in many ways, species unique. Only catecholamines, insulin and natriuretic peptides have pronounced acute effects. Catecholamines influence lipolysis through four different adrenoceptor subtypes, in contrast to rodents where only one subtype (beta(3)) is of major importance. There are regional variations in adipocyte lipolysis leading to more release of FAs from the visceral than subcutaneous adipose tissue during hormone stimulation (insulin, catecholamines). Since, only visceral fat is linked to the liver (by the portal vein), alterations in visceral adipocyte tissue lipolysis have direct effects on the liver through portal FA release. The regional variations in lipolysis are further enhanced in obesity and polycystic ovarian syndrome, and are of importance for dyslipidaemia, hyperinsulinaemia and glucose intolerance in these conditions. There is a marked elevation of circulating FA levels among the obese, which may be due to enhanced production of tumour necrosis factor alpha in adipose tissue. This cytokine stimulates lipolysis through so-called MAP kinases. Pharmacological agents in clinical practice such as nicotinic acid and glitazones exert lipid-lowering and glucose-lowering effects, respectively, by decreasing FA output from the adipose tissue. This review covers the biochemistry, regulation and clinical aspects of human fat cell lipolysis.

PMID: 16311212 [PubMed - in process]


[Innovative therapies in metabolic diseases: ezetimibe (Ezetrol), nicotinic acid (Niaspan), acids omega-3 (Omacor), rimonabant (Acomplia)]


Ducobu J.

Service de Medecine Interne, C.H.U. Tivoli, La Louviere.

In the field of dyslipidemia and metabolic syndrome, four innovative therapies are reviewed: Ezetimibe (Ezetrol) is a selective cholesterol absorption inhibitor. Co-administration of ezetimibe with low dose of statins shows LDL lowering comparable to that of the highest dose of the respective statin alone. Combination therapy helps more patients in achieving target LDL-cholesterol. Nicotinic acid (Niacin) favourably modifies all lipoprotein level (including Lp(a)). Extended release niacin (Niaspana) is a new galenic form, with less side effects (flushing and hepatotoxicity) than the native nicotinic acid. This new preparation represents an effective option in the management of dyslipidemia. The polyunsatured fatty acids (PUFA) omega-3 (Omacor) decreases cardiovascular deaths and mainly fatal arrhythmias after myocardial infarction. Their favourable effects are linked mainly to their anti-inflammatory and antiarrhythmic properties. The PUFA omega-3 could be added to the secondary prevention after myocardial infarction. The blockade of the endocannabinoid system by a specific inhibitor of CB1 receptor (rimonabant or Acomplia) decreases food intake and weight and increases adiponectin and insulin sensitivity. Clinical studies on obesity and tobacco dependence are very encouraging.

PMID: 16240893 [PubMed - indexed for MEDLINE]

 

[AX_Ryan]

Looks like mine links did not work. Just search pubmed for the items.

 

[EL GAUCHO]

Thanks guys..good info here!

 

[Cynical Simian]

I assume you're already checking out PubMed. Here's another good database on which you can access full texts of some articles in addition to the abstracts:

http://highwire.stanford.edu/lists/freeart.dtl

 

[Lifterforlife]

That is a good one. Another that is good...... http://www.jssm.org/

 

[EL GAUCHO]

Thanks again guys...good stuff.