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Lipopolysaccharide-induced leptin release is neurally controlled.

Discussion in 'Other Health News and Research' started by Ema, Feb 28, 2014.

  1. Ema

    Ema Senior Member

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    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC64748/

    More decreased dopamine and increased prolactin...clearly an influence on metabolism.

     
  2. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    being a dam boy or a girl can always throw a spanner in the works when it comes to alot of research on hormones and neurotransmitters.

    Probably 20yrs ago there was research on beta 3 receptor, prior to this only beta 1 and 2 receptors were thought to exist. What they found was some asthma medications could help people lose weight by speeding up their metabolisms, further research found a beta 3 receptor which is supposedly involved in fat metabolism. Just though i would mention this as it may fit into this interlocking web of hormones and neurotransmitters especially insulin/leptin sensitivity and maybe mito function, may play a role with carnitine??
     
  3. Ema

    Ema Senior Member

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    Thought I would re-post this study here too:

    J Transl Med. 2013 Apr 9;11:93. doi: 10.1186/1479-5876-11-93.
    Daily cytokine fluctuations, driven by leptin, are associated with fatigue severity in chronic fatigue syndrome: evidence of inflammatory pathology.
    Stringer EA1, Baker KS, Carroll IR, Montoya JG, Chu L, Maecker HT, Younger JW.
    Author information
    • 1Department of Anesthesiology, Stanford University School of Medicine, Stanford, CA 94304, USA.
    Abstract
    BACKGROUND:
    Chronic fatigue syndrome (CFS) is a debilitating disorder characterized by persistent fatigue that is not alleviated by rest. The lack of a clearly identified underlying mechanism has hindered the development of effective treatments. Studies have demonstrated elevated levels of inflammatory factors in patients with CFS, but findings are contradictory across studies and no biomarkers have been consistently supported. Single time-point approaches potentially overlook important features of CFS, such as fluctuations in fatigue severity. We have observed that individuals with CFS demonstrate significant day-to-day variability in their fatigue severity.

    METHODS:
    Therefore, to complement previous studies, we implemented a novel longitudinal study design to investigate the role of cytokines in CFS pathophysiology. Ten women meeting the Fukuda diagnostic criteria for CFS and ten healthy age- and body mass index (BMI)-matched women underwent 25 consecutive days of blood draws and self-reporting of symptom severity. A 51-plex cytokine panel via Luminex was performed for each of the 500 serum samples collected. Our primary hypothesis was that daily fatigue severity would be significantly correlated with the inflammatory adipokine leptin, in the women with CFS and not in the healthy control women. As a post-hoc analysis, a machine learning algorithm using all 51 cytokines was implemented to determine whether immune factors could distinguish high from low fatigue days.

    RESULTS:
    Self-reported fatigue severity was significantly correlated with leptin levels in six of the participants with CFS and one healthy control, supporting our primary hypothesis. The machine learning algorithm distinguished high from low fatigue days in the CFS group with 78.3% accuracy.

    CONCLUSIONS:
    Our results support the role of cytokines in the pathophysiology of CFS.

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    23570606

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    PMC3637529

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  4. Ema

    Ema Senior Member

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    I know theophylline works for this by blocking adenosine. And I guess these beta receptors too?

    Am J Physiol Cell Physiol. 2002 Jul;283(1):C244-50.
    Mechanisms of leptin secretion from white adipocytes.
    Cammisotto PG1, Bukowiecki LJ.
    Author information

    Abstract
    The mechanisms regulating leptin secretion were investigated in isolated rat white adipocytes. Insulin (1-100 nM) linearly stimulated leptin secretion from incubated adipocytes for at least 2 h. The adrenergic agonists norepinephrine, isoproterenol (two nonselective beta-agonists), or CL-316243 (potent beta3) all inhibited insulin (10 nM)-stimulated leptin release. The inhibitory effects of norepinephrine and isoproterenol could be reversed not only by the nonselective antagonist propranolol but also by the selective antagonists ICI-89406 (beta1) or ICI-118551 (beta2), the beta2-antagonist being less effective than the beta1. Insulin-stimulated leptin secretion could also be inhibited by a series of agents increasing intracellular cAMP levels, such as lipolytic hormones (ACTH and thyrotropin-stimulating hormone), various nonhydrolyzable cAMP analogs, pertussis toxin, forskolin, methylxanthines (caffeine, theophylline, IBMX), and specific inhibitors of phosphodiesterase III (imazodan, milrinone, and amrinone). Significantly, antilipolytic agents other than insulin (adenosine, nicotinic acid, acipimox, and orthovanadate) did not mimic the acute stimulatory effects of insulin on leptin secretion under these conditions. We conclude that norepinephrine specifically inhibits insulin-stimulated leptin secretion not only via the low-affinity beta3-adrenoceptors but also via the high-affinity beta1/beta2-adrenoceptors. Moreover, it is suggested that 1) activation of phosphodiesterase III by insulin represents an important metabolic step in stimulation of leptin secretion, and 2) lipolytic hormones competitively counterregulate the stimulatory effects of insulin by activating the adenylate cyclase system.
     
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  5. Ema

    Ema Senior Member

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    This increasing cellular cAMP always comes up too in terms of mitochondria and energy generation.

    I think I posted a study under Hormones showing how glucocorticoids do this, and I know we've talked about forskolin before as increasing cAMP.

    That's also how that PQQ supp from Life Ext is supposed to work as well, I think, at least in part.

    I'm currently working under the assumption (from other studies) that part of the problem is interferon gamma not turning "off" properly and thus allowing the infection to turn chronic (by not producing antibodies properly) so this is kind of interesting as well.

    Buhner says something similar...that the Th1 response never properly converts to the Th2 response which is what perpetuates chronic disease in some and interferon gamma may be one reason why that happens.

    http://onlinelibrary.wiley.com/doi/10.1002/glia.440140204/abstract

    Maybe I just like that they called IFN-g "obnoxious" in a scientific journal. :)
     
    Last edited: Mar 1, 2014
  6. Ema

    Ema Senior Member

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    And that appears to possibly be why some go on to develop chronic Lyme, while others can more rapidly clear an infection.

    HLA-DR alleles determine responsiveness to Borrelia burgdoferi antigens
    Bettina Panagiota Iliopoulou, Mireia Guerau-de-Arellano, and Brigitte T. Huber. Arthritis Rheum. 2009 December; 60(12): 3831–3840.

    Source:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828865

     
    Last edited: Mar 1, 2014
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  7. rosie26

    rosie26 Senior Member

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    @Ema if you come across any more research about Bacterial Lipopolysaccharide. I would be most grateful. I don't know good research from not so good. Many thanks.
     
    Last edited: Aug 18, 2014
    Ema likes this.

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