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  1. #1
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    Insulin Resistance Is Associated with Impaired Nitric Oxide

    Insulin Resistance Is Associated with Impaired Nitric Oxide Synthase Activity in Skeletal Muscle of Type 2 Diabetic Subjects

    Abstract

    Type 2 diabetes is an insulin-resistant state characterized by hyperinsulinemia and accelerated atherosclerosis. In vitro and in vivo studies in rodents have suggested that nitric oxide generation plays an important role in glucose transport and insulin action. We determined nitric oxide synthase (NOS) activity in skeletal muscle of 10 type 2 diabetic (hemoglobin A1C = 6.8 ± 0.1%) and 11 control subjects under basal conditions and during an 80 mU/m2·min euglycemic insulin clamp performed with vastus lateralis muscle biopsies before and after 4 h of insulin. In diabetics, insulin-stimulated glucose disposal (Rd) was reduced by 50%, compared with controls (5.4 ± 0.3 vs. 10.4 ± 0.5 mg/kg·min, P < 0.01). Basal NOS activity was markedly reduced in the diabetic group (101 ± 33 vs. 457 ± 164 pmol/min·mg protein, P < 0.05). In response to insulin, NOS activity increased 2.5-fold in controls after 4 h (934 ± 282 pmol/min·mg protein, P < 0.05 vs. basal), whereas insulin failed to stimulate NOS activity in diabetics (86 ± 28 pmol/min·mg protein, P = NS from basal). Basal NOS protein content in muscle was similar in controls and diabetics and did not change following insulin. In controls, insulin-stimulated NOS activity correlated inversely with fasting plasma insulin concentration (r = ?0.58, P = 0.05) and positively with Rd (r = 0.71, P = 0.03). In control and diabetic groups collectively, Rd correlated with insulin-stimulated NOS activity (r = 0.52, P = 0.02). We conclude that basal and insulin-stimulated muscle NOS activity is impaired in well-controlled type 2 diabetic subjects, and the defect in insulin-stimulated NOS activity correlates closely with the severity of insulin resistance. These results suggest that impaired NOS activity may play an important role in the insulin resistance in type 2 diabetic individuals.


    http://jcem.endojournals.org/content/90/2/1100.short

  2. #2
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    Re: Insulin Resistance Is Associated with Impaired Nitric Oxide

    This is why Insulin Resistance is linked to baldness.. Look how Metanx works.. and what high blood sugar can do to your body. This is also explain why Minoxidil works good locally, it mimics Nitric Oxide locally.
    [youtube:2xt62l1y]http://www.youtube.com/watch?v=JvN_9XmDsdA[/youtube:2xt62l1y]

  3. #3
    Senior Member Jacob's Avatar
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    Re: Insulin Resistance Is Associated with Impaired Nitric Oxide

    How about using nitroglycerin topically? A small area at a time..of course.

    Nitroglycerin, which is locally metabolized to nitric oxide,
    Hmmmm...
    Nitroglycerin applied topically increases bone formation

  4. #4
    Senior Member Jacob's Avatar
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    Re: Insulin Resistance Is Associated with Impaired Nitric Oxide

    Just did a search..and it seems you've tried it...?

  5. #5
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    Re: Insulin Resistance Is Associated with Impaired Nitric Oxide

    Quote Originally Posted by Jacob
    Just did a search..and it seems you've tried it...?

    Yes.. still have a lot.. barely using it.. it is really hardcore stuff.. hearbeats.. dark circles... the problem is internally.. I am on Minox and Miconazole Nitrate 2%topically for now, still looking for a cheap 4% Mico alternative for better results...I am taking this internally also with a lot of other antioxidants and anti inflammatory.

    http://www.iherb.com/Metabolic-Maintena ... 38360?at=0

    L-methylfolate is the main ingredient in MetanX. It reverses Endothelial dysfunction. way more mg than Metanx also.

    Diabetes Metab Res Rev. 2006 Nov-Dec;22(6):423-36.
    Insulin resistance and endothelial dysfunction: the road map to cardiovascular diseases.
    Cersosimo E, DeFronzo RA.
    Source

    Division of Diabetes, Department of Medicine, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA. Eugenio.Cersosimo@uhs-sa.com
    Abstract

    Cardiovascular disease affects approximately 60% of the adult population over the age of 65 and represents the number one cause of death in the United States. Coronary atherosclerosis is responsible for the vast majority of the cardiovascular events, and a number of cardiovascular risk factors have been identified. In recent years, it has become clear that insulin resistance and endothelial dysfunction play a central role in the pathogenesis of atherosclerosis. Much evidence supports the presence of insulin resistance as the fundamental pathophysiologic disturbance responsible for the cluster of metabolic and cardiovascular disorders, known collectively as the metabolic syndrome. Endothelial dysfunction is an important component of the metabolic or insulin resistance syndrome and this is demonstrated by inadequate vasodilation and/or paradoxical vasoconstriction in coronary and peripheral arteries in response to stimuli that release nitric oxide (NO). Deficiency of endothelial-derived NO is believed to be the primary defect that links insulin resistance and endothelial dysfunction. NO deficiency results from decreased synthesis and/or release, in combination with exaggerated consumption in tissues by high levels of reactive oxygen (ROS) and nitrogen (RNS) species, which are produced by cellular disturbances in glucose and lipid metabolism. Endothelial dysfunction contributes to impaired insulin action, by altering the transcapillary passage of insulin to target tissues. Reduced expansion of the capillary network, with attenuation of microcirculatory blood flow to metabolically active tissues, contributes to the impairment of insulin-stimulated glucose and lipid metabolism. This establishes a reverberating negative feedback cycle in which progressive endothelial dysfunction and disturbances in glucose and lipid metabolism develop secondary to the insulin resistance. Vascular damage, which results from lipid deposition and oxidative stress to the vessel wall, triggers an inflammatory reaction, and the release of chemoattractants and cytokines worsens the insulin resistance and endothelial dysfunction.From the clinical standpoint, much experimental evidence supports the concept that therapies that improve insulin resistance and endothelial dysfunction reduce cardiovascular morbidity and mortality. Moreover, interventional strategies that reduce insulin resistance ameliorate endothelial dysfunction, while interventions that improve tissue sensitivity to insulin enhance vascular endothelial function. There is general agreement that aggressive therapy aimed simultaneously at improving insulin-mediated glucose/lipid metabolism and endothelial dysfunction represents an important strategy in preventing/delaying the appearance of atherosclerosis. Interventions that 1 correct carbohydrate and lipid metabolism, 2 improve insulin resistance, 3 reduce blood pressure and restore vascular reactivity, and 4 attenuate procoagulant and inflammatory responses in adults with a high risk of developing cardiovascular disease reduce cardiovascular morbidity and mortality. Whether these benefits hold when the same prevention strategies are applied to younger, high-risk individuals remains to be determined.

    The impact of insulin resistance on endothelial function, progenitor cells and repair

    Richard M Cubbon
    The Academic Unit of Cardiovascular Medicine, The LIGHT Laboratories, University of Leeds, Clarendon Way, Leeds, LS2 9JT, UK.

    Adil Rajwani
    The Academic Unit of Cardiovascular Medicine, The LIGHT Laboratories, University of Leeds, Clarendon Way, Leeds, LS2 9JT, UK.

    Stephen B Wheatcroft
    The Academic Unit of Cardiovascular Medicine, The LIGHT Laboratories, University of Leeds, Clarendon Way, Leeds, LS2 9JT, UK.

    Abstract

    The structural and functional integrity of the vascular endothelium plays a critical role in vascular homeo-stasis. Insulin resistance, an important risk factor for cardiovascular disease, is thought to promote atherosclerosis through a reciprocal relationship with endothelial dysfunction. In health, cumulative damage to endothelial cells incurred by exposure to risk factors is mitigated by endogenous reparative processes. Disruption of the balance between endothelial damage and repair may mediate atherosclerotic progression. Bone marrow-derived ‘endothelial progenitor cells' (EPC) have been identified as significant contributors to endogenous vascular repair. Insulin resistance is associated with a spectrum of biochemical abnormalities which have the potential to reduce the availability of EPCs and diminish their capacity for vascular repair. Many lifestyle and pharmacological interventions which improve insulin resistance also increase the numbers and functionality of EPCs. Cell-based therapies may also hold promise for the prevention and treatment of cardiovascular disease.

    Basic Science for Clinicians

    Reciprocal Relationships Between Insulin Resistance and Endothelial Dysfunction
    Molecular and Pathophysiological Mechanisms

    Jeong-a Kim, PhD;
    Monica Montagnani, MD, PhD;
    Kwang Kon Koh, MD;
    Michael J. Quon, MD, PhD

    + Author Affiliations

    From the Diabetes Unit, National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Md (J.K., M.J.Q.); Department of Pharmacology and Human Physiology, Section of Pharmacology, University of Bari Medical School, Bari, Italy (M.M.); and the Division of Cardiology, Gil Heart Center, Gachon Medical School, Incheon, Korea (K.K.K.).

    Correspondence to Michael J. Quon, MD, PhD, Chief, Diabetes Unit, NCCAM, NIH, 10 Center Dr, Building 10, Room 6C-205, Bethesda, MD 20892-1632. E-mail quonm@nih.gov

    Abstract

    Endothelial dysfunction contributes to cardiovascular diseases, including hypertension, atherosclerosis, and coronary artery disease, which are also characterized by insulin resistance. Insulin resistance is a hallmark of metabolic disorders, including type 2 diabetes mellitus and obesity, which are also characterized by endothelial dysfunction. Metabolic actions of insulin to promote glucose disposal are augmented by vascular actions of insulin in endothelium to stimulate production of the vasodilator nitric oxide (NO). Indeed, NO-dependent increases in blood flow to skeletal muscle account for 25% to 40% of the increase in glucose uptake in response to insulin stimulation. Phosphatidylinositol 3-kinase–dependent insulin-signaling pathways in endothelium related to production of NO share striking similarities with metabolic pathways in skeletal muscle that promote glucose uptake. Other distinct nonmetabolic branches of insulin-signaling pathways regulate secretion of the vasoconstrictor endothelin-1 in endothelium. Metabolic insulin resistance is characterized by pathway-specific impairment in phosphatidylinositol 3-kinase–dependent signaling, which in endothelium may cause imbalance between production of NO and secretion of endothelin-1, leading to decreased blood flow, which worsens insulin resistance. Therapeutic interventions in animal models and human studies have demonstrated that improving endothelial function ameliorates insulin resistance, whereas improving insulin sensitivity ameliorates endothelial dysfunction. Taken together, cellular, physiological, clinical, and epidemiological studies strongly support a reciprocal relationship between endothelial dysfunction and insulin resistance that helps to link cardiovascular and metabolic diseases. In the present review, we discuss pathophysiological mechanisms, including inflammatory processes, that couple endothelial dysfunction with insulin resistance and emphasize important therapeutic implications.

  6. #6
    Senior Member Jacob's Avatar
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    Re: Insulin Resistance Is Associated with Impaired Nitric Oxide

    on the nitro...yeah..I was told one could get a headache just using a finger to apply it on someone. I was thinking maybe just a small area each day or something..but

    That L-methylfolate looks very interesting. That one is expensive though! I see LEF(and Doctor's best etc) uses this brand: http://www.quatrefolic.com/
    and http://www.webwire.com/ViewPressRel.asp?aId=138022 but not the mg you get with the one you posted. Maybe they too use the same stuff.

  7. #7
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    Re: Insulin Resistance Is Associated with Impaired Nitric Oxide

    Bad ass Jacob! BAD ASS!!
    2- Greater bioavailability than the 5-methytetrahydrofolate calcium salt form
    3- Able to penetrate cells without being metabolized

    BTW Jacob! you can get L-methylfolate 10 mg cheaper on Amazon.com http://www.amazon.com/Metabolic-Mainten ... 087&sr=8-7

    I wish I can find a legit Folic acid supplement in a liposomal formulation. That would be the best.

    A Must read about Nitric Oxide : http://www.lmreview.com/articles/view/l ... e-part-II/

  8. #8
    Senior Member Jacob's Avatar
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    Re: Insulin Resistance Is Associated with Impaired Nitric Oxide

    I think I've seen liposomal Foilic acid in combo products..B vits...

    I may try that Quatrefolic stuff for awhile.

  9. #9
    Senior Member Jacob's Avatar
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    Re: Insulin Resistance Is Associated with Impaired Nitric Oxide

    Contacted Quatrefolic and got this list:


    Aceto Corporation

    Allergy Research Group

    Bionutragen LLC

    Biotics Research Corporation

    Bio Tech Pharmacal Inc.

    Clarks Pharmacy

    Doctors Best

    Factors Group

    Free Life Vitonomy LLC

    Garden State Nutritionals

    Gemini Pharmaceuticals Inc.

    Health Wright Products Inc.

    LifeExtension

    Nature's Value Inc.

    NOW Foods

    Pro-Form Laboratories

    Progressive Laboratories Inc.

    Robinson Pharma, Inc.

    Schiff Nutrition International

    Swanson Nutritionals

    Thorne Research Inc.

    United Pharma

    Vitaganic Inc.

    WowNow Nutritionals, Inc
    They're companies that either purchased it for making their own branded products...or are contract manufacturers. Swanson has 3 different products containing it(800mcg): http://www.swansonvitamins.com/Searc...vel1&x=20&y=17 Haven't looked into the others yet.

  10. #10
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    Re: Insulin Resistance Is Associated with Impaired Nitric Oxide

    Insulin resistance: potential role of the endogenous nitric oxide synthase inhibitor ADMA

    The insulin resistance syndrome (IRS) is considered to be a new target of risk-reduction therapy. The IRS is a cluster of closely associated and interdependent abnormalities and clinical outcomes that occur more commonly in insulin-resistant/hyperinsulinemic individuals. This syndrome predisposes individuals to type 2 diabetes, cardiovascular diseases, essential hypertension, certain forms of cancer, polycystic ovary syndrome, nonalcoholic fatty liver disease, and sleep apnea. In patients at high risk for cardiovascular diseases, endothelial dysfunction is observed in morphologically intact vessels even before the onset of clinically manifest vascular disease. Indeed, there are several lines of evidence that indicate that endothelial function is compromised in situations where there is reduced sensitivity to endogenous insulin. It is well established that a decreased bioavailability of nitric oxide (NO) contributes to endothelial dysfunction. Furthermore, NO may modulate insulin sensitivity. Activation of NO synthase (NOS) augments blood flow to insulin-sensitive tissues (i.e. skeletal muscle, liver, adipose tissue), and its activity is impaired in insulin resistance. Inhibition of NOS reduces the microvascular delivery of nutrients and blunts insulin-stimulated glucose uptake in skeletal muscle. Furthermore, induction of hypertension by administration of the NOS inhibitor NG-monomethyl-L-arginine is also associated with insulin resistance in rats. Increased levels of asymmetric dimethylarginine (ADMA) are associated with endothelial vasodilator dysfunction and increased risk of cardiovascular diseases. An intriguing relationship exists between insulin resistance and ADMA. Plasma levels of ADMA are positively correlated with insulin resistance in nondiabetic, normotensive people. New basic research insights that provide possible mechanisms underlying the development of insulin resistance in the setting of impaired NO bioavailability will be discussed.

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