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Nathan Goodyear

Obesity and testicular function. [Mol Cell Endocrinol. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...19540307

obesity leydig cells Testosterone low T low Testosterone T SHBG LH leptin men male hormone hormones

shared by Nathan Goodyear on 04 Sep 14 - No Cached
  • Nathan Goodyear on 04 Sep 14
     
    This article, here only abstract available, points to low Testosterone as the effect and not the cause.  The cause being obesity.  An interesting association between leptin and low T is found.  Leptin is a hormone produced from adipocytes, this study found leptin receptors in the leydig cells of testes.  Thus, increased leptin production from increased abdominal adiposity can result in a decrease in 17,20 lyase activity and thus a direct inhibition of leydig cell Testosterone production.
Nathan Goodyear

Androgen Therapy Improves Insulin Sensitivity and Decreases Leptin Level in Healthy Adu... - 0 views

care.diabetesjournals.org/...2149.extract

low T low Testosterone leptin obesity Testosterone therapy insulin resistance

shared by Nathan Goodyear on 22 Oct 14 - No Cached
  • Nathan Goodyear on 22 Oct 14
     
    Three month study of men with low T, found that Testosterone therapy improved insulin sensitivity and reduced leptin levels.  The group of men here were described as "healthy, non-obese men".   Remember, low T is a biomarker of poor health in men, so the authors statement about the study group is inaccurate.  This also points to a relatively quick metabolic effect by Testosterone and a direct effect on insulin receptor effect and adipocyte leptin release.
Nathan Goodyear

Hypoxia Decreases Insulin Signaling Pathways in Adipocytes | Diabetes - 0 views

diabetes.diabetesjournals.org/...95

IL-6 obesity hypoxia HIF-1alpha insulin adipocytes

shared by Nathan Goodyear on 14 Jan 21 - No Cached
  • Nathan Goodyear on 14 Jan 21
     
    Hypoxia, via HIF-1alpha, inhibits Insulin:insulin receptor signaling, and inhibits IRS signaling.
Nathan Goodyear

Adipocyte Signaling and Lipid Homeostasis - 0 views

circres.ahajournals.org/...1042.long

insulin resistance IR insulin lipid metabolism lipids adipose tissue adipose tissue fatty acids

shared by Nathan Goodyear on 04 Mar 13 - No Cached
  • Nathan Goodyear on 04 Mar 13
     
    great review of how insulin resistance effects lipid metabolism homeostasis.
Nathan Goodyear

ScienceDirect.com - Cell Metabolism - Estrogen Receptors and the Metabolic Network - 0 views

www.sciencedirect.com/...S1550413111003123

ER-alpha ER-beta estrogen receptor receptors metabolic syndrome MetS hormone hormones

shared by Nathan Goodyear on 11 Oct 12 - No Cached
  • The pro-opiomelanocortin (POMC) neurons have an anorexigenic action and, when activated, reduce food intake through the release of two peptides, α-melanocyte-stimulating hormone (α-MSH) and cocaine-and-amphetamine-regulated transcripts (CART). The neuropeptide Y (NPY) neurons, on the other hand, release NPY hormone and agouti gene-related protein (AgRP), which prevent the binding of α-MSH to MC3R and MC4R, increasing food intake
  • This suggests that the central anorexic effects of E2 may occur via ERβ
  • The main hypothalamic areas involved in food intake and satiety are the arcuate nucleus (ARC), the lateral hypothalamus (LH), the paraventricular nucleus (PVN), the ventromedial hypothalamus (VMH), and the dorsomedial hypothalamus (DMH)
  • ...22 more annotations...
  • Leptin is a potent anorexigenic and catabolic hormone secreted by adipose cells that reduces food intake and increases energy expenditure
  • E2 not only modulates leptin receptor mRNA in the ARC and VMH, but also increases hypothalamic sensitivity to leptin, altering peripheral fat distribution
  • ghrelin. It acts on growth hormone secretagogue receptors (GHSR1a) located in the ARC and is a potent stimulator of food intake
  • It thus appears that of the two ERs, ERα plays a predominant role in the CNS regulation of lipid and carbohydrate homeostasis.
  • Both ERs have been identified in the ARC
  • Stimulation of MCH neurons increases food intake and fat accumulation while its inhibition leads to decreased food intake and reduced fat accumulation.
  • Both ERs have been identified in the LH
  • both ERs have been identified in this nucleus
  • The PVN is the region of the hypothalamus with the highest expression of ERβ and is reported to be weakly ERα positive
  • The VMH is ERα regulated
  • Skeletal muscle is responsible for 75% of the insulin-induced glucose uptake in the body
  • GLUT4 is highly expressed in muscle and represents a rate-limiting step in the insulin-induced glucose uptake
  • data suggest that in the physiological range, E2 is beneficial for insulin sensitivity, whereas hypo- or hyperestrogenism is related to insulin resistance
  • In aging female rats, E2 treatment improves glucose homeostasis mainly through its ability to increase muscle GLUT4 content on the cell membrane
  • It is evident that ERα and ERβ have distinct actions and that much more research is needed to clearly identify the function of each receptor in muscle.
  • E2 prevents accumulation of visceral fat, increases central sensitivity to leptin, increases the expression of insulin receptors in adipocytes, and decreases the lipogenic activity of lipoprotein lipase in adipose tissue
  • In rats, ovariectomy increases body weight, intra-abdominal fat, fasting glucose and insulin levels, and insulin resistance followed by decreased phosphorylation of AMPK and its substrate acetyl-CoA carboxylase in adipose tissue
  • decreased adiponectin, PPARγ coactivator-1α (PGC-1α), and uncoupling protein 2 (UCP2) and increased resistin
  • Men with aromatase deficiency have truncal obesity, elevated blood lipids, and severe insulin resistance
  • Although not all studies are in agreement, polymorphisms of ERα in humans have been associated with risk factors for CVDs
  • Human subcutaneous and visceral adipose tissues express both ERα and ERβ, whereas only ERα mRNA has been identified in brown adipose tissue
  • suggesting that ERα is the main regulator of GLUT4 expression in adipose tissue
  • Nathan Goodyear on 11 Oct 12
     
    very nice article that looks at the balance of ER-alpha/ER-beta and their role in metabolic syndrome.  This article discusses the balance of  these receptors are tissue dependent in their effect.  I like their conclusion: "...but these mechanisms will never be completely understood if they are not considered in the context of a whole system.
Nathan Goodyear

Minireview: Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up - 0 views

endo.endojournals.org/...4109.full

inflammation obesity overweight hypothalamus HPA

shared by Nathan Goodyear on 04 Oct 12 - No Cached
  • Leptin, secreted by adipocytes in proportion to body fat mass
  • The saturated fatty acid palmitate (16:0) induces NF-κB signaling through a TLR4-dependent mechanism
  • 18:0 (stearic) and longer saturated fatty acids as well as linolenic acid (18:3) increased proinflammatory cytokines, ER stress markers, and TLR4 activation
  • ...6 more annotations...
  • (SOCS)-3. A member of a protein family originally characterized as negative feedback regulators of inflammation (13, 37), SOCS3 inhibits insulin and leptin signaling
  • IKKβ signaling in discrete neuronal subsets appears to be required for both hypothalamic inflammation and excess weight gain to occur during HF feeding
  • the paradoxical observation that hyperphagia and weight gain occur when hypothalamic inflammation is induced by HF feeding, yet when it occurs in response to systemic or local inflammatory processes (e.g. administration of endotoxin), anorexia and weight loss are the rule
  • , serves as a circulating signal of energy stores in part by providing feedback inhibition of hypothalamic orexigenic pathways [e.g. neurons that express neuropeptide Y and agouti-related peptide (AgRP)]
  • and stimulating anorexigenic neurons
  • signals from Toll-like receptors (TLRs), evolutionarily conserved pattern recognition molecules critical for detecting pathogens, amplified through signaling intermediates such as MyD88 activate the inhibitor of κB-kinase-β (IKKβ)/nuclear factor-κB (NF-κB), c-Jun N-terminal kinase (Jnk) and other intracellular inflammatory signals in response to stimulation by circulating saturated fatty acids
  • Nathan Goodyear on 04 Oct 12
     
    great read on the current understanding of how obesity and resultant inflammation disrupts hypothalamic function.
Nathan Goodyear

Gender and sex hormones in multiple sclerosis pathology and therapy - 0 views

www.ncbi.nlm.nih.gov/...PMC2689399

hormones MS multiple Sclerosis Estriol progesterone

shared by Nathan Goodyear on 11 Jan 17 - No Cached
  • It is now well recognized that the disease manifestation is reduced in pregnant women with relapsing-remitting MS
  • This occurs particularly during the third trimester when levels of estrogens (estradiol and estriol) and progesterone (see Table 2) are elevated up to about 20 times
  • This seems well correlated with a decrease in active white matter lesions detected by MRI
  • ...12 more annotations...
  • This clinical improvement is however followed by temporary rebound exacerbations at post-partum, when the hormone levels decline
  • a shift from Th1 to Th2 immune response, expansion of suppressive regulatory T lymphocytes and decrease in the number of circulating CD16+ natural killer (NK)-cells
  • Th1 lymphocytes secrete proinflammatory cytokines (e.g. IL-2, IFNgamma, lymphotoxin) while Th2 cells secrete anti-inflammatory cytokines (e.g. IL-4, IL-5, IL-10), which favor humoral-mediated responses
  • Th2 cytokines are associated with down-regulation of Th1 cytokines and this Th2 shift is believed to provide protection from allograft rejection during pregnancy as well as from Th1-mediated autoimmune disease
  • it is worth noting that the levels of other hormones with anti-inflammatory activity (1,25-dihydroxy-vitamin D3, norepinephrine, cortisol) also increase by 2 to 4 times during late pregnancy
  • 1,25-dihydroxy vitamin D3 induces regulatory T-cell function important for development of self-tolerance
  • breast-feeding does not alter the relapse rate in women with MS
  • Leptin is a pleiotropic hormone produced primarily by adipocytes but also by T lymphocytes and neurons
  • Several lines of evidence indicate that leptin contributes to EAE/MS pathogenesis, influencing its onset and clinical severity, by acting as a proinflammatory cytokine which promotes regulatory T cell (Treg) anergy and hyporesponsiveness, resulting in increased Th1 (TNFalpha, INFgamma) and reduced Th2 (IL-4) cytokine production
  • circulating leptin levels are increased in relapsing-remitting MS patients (men and women analyzed together) while the CD4+CD25+Treg population decreases
  • As the leptin plasma concentrations are proportional to the amount of fat tissue, obese/overweight individuals produce higher levels of leptin
  • Nielsen et al found that estradiol and progesterone exert neuroprotection against glutamate neurotoxicity, while MPA antagonizes the neuroprotective effect of estradiol and exacerbated neuron death induced by glutamate excitotoxicity
  • Nathan Goodyear on 11 Jan 17
     
    very good review of the differences in MS and hormones between the sexes.
Nathan Goodyear

Effect of DHEA-sulfate on adiponectin gene expression in adipose tissue from different ... - 0 views

www.eje.org/...593.full

DHEA-S DHEAS adiponectin adipose tissue adipocytes fat cells insulin resistance obesity

shared by Nathan Goodyear on 17 Mar 12 - No Cached
  • Nathan Goodyear on 17 Mar 12
     
    DHEA-S shown to increase genetic expression of adiponectin in human adipose tissue.  This has enormous implications on the link between DHEA and insulin resistance induce obesity. This is a peripheral tissue problem, not a central problem.
Nathan Goodyear

Dehydroepiandrosterone reduces preadipocyte proliferation via androgen receptor - 0 views

ajpendo.physiology.org/...E694.abstract

DHEA obesity adipose tissue adipocytes fat diabetes androgen receptor

shared by Nathan Goodyear on 17 Mar 12 - No Cached
  • Nathan Goodyear on 17 Mar 12
     
    DHEA reduces preadipocytes growth through the androgen receptor.
Nathan Goodyear

Elevated Levels of Interleukin 6 Are Reduced in Serum and Subcutaneous Adipose Tissue o... - 0 views

jcem.endojournals.org/...3338.full

weight loss overweight obesity adipose tissue adipocytes IL-6 leptin inflammation

shared by Nathan Goodyear on 15 Mar 12 - No Cached
  • Nathan Goodyear on 15 Mar 12
     
    weight loss resulted in reduction in IL-6 and leptin.  The reduction of IL-6 reflects a decrease in inflammation. The reduction in leptin reflects an improved leptin sensitivity.
Nathan Goodyear

Adipose Tissue: The New Endocrine Organ? - 0 views

www.springerlink.com/...fulltext.pdf

fat obesity adipocytokines cytokines adipocytes overweight inflammation inflammatory adipokines chemokines

shared by Nathan Goodyear on 31 May 12 - No Cached
  • Nathan Goodyear on 31 May 12
     
    fat and obesity becomes a hormone, inflammatory producing organ. Great read. You must be healthy to lose weight, not lose weigh to be healthy. The "fat" in obesity has been link to many of the chronic diseases of aging
Nathan Goodyear

Access : FFA-Induced Adipocyte Inflammation and Insulin Resistance: Involvement of ER S... - 0 views

www.nature.com/...oby2010200a.html

FFA inflammation overweight obesity free fatty acids insulin resistance IKK-Beta endoplasmic reticulum stress

shared by Nathan Goodyear on 21 Dec 11 - No Cached
  • Nathan Goodyear on 21 Dec 11
     
    elevated FFA (free-fatty acids) shown to produce inflammation and insulin resistance through endoplasmic reticulum stress.  The main target in this pathway is IKK-Beta overexpression.
Nathan Goodyear

Figure 2 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

www.nature.com/...nrm2391_F2.html

obesity insulin resistance diabetes inflammation triglyceride metabolsim FFA TNF-alpha

shared by Nathan Goodyear on 22 Dec 11 - No Cached
  • Nathan Goodyear on 22 Dec 11
     
    chronic, not acute, inflammation disrupts normal triglyceride metabolism and results in increased FFA
Nathan Goodyear

Figure 3 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

www.nature.com/...nrm2391_F3.html

obesity insulin resistance diabetes TNF-alpha PPAR free fatty acids FFA inflammation

shared by Nathan Goodyear on 22 Dec 11 - No Cached
  • Nathan Goodyear on 22 Dec 11
     
    TNF-alpha downregulates PPAR and increases FFA
Nathan Goodyear

Figure 5 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

www.nature.com/...nrm2391_F5.html

obesity insulin resistance diabetes TNF-alpha PPAR free fatty acids FFA inflammation

shared by Nathan Goodyear on 22 Dec 11 - No Cached
  • Nathan Goodyear on 22 Dec 11
     
    proposed TNF-alpha downregulation of PPAR and resultant increase in FFA and thus inflammation, insulin resistance, diabetes...
Nathan Goodyear

Figure 4 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

www.nature.com/...nrm2391_F4.html

obesity insulin resistance diabetes inflammation TNF-alpha

shared by Nathan Goodyear on 22 Dec 11 - No Cached
  • Nathan Goodyear on 22 Dec 11
     
    nice diagram of how inflammation, particularily TNF-alpha in this case, promotes insulin resistance
Nathan Goodyear

Fatty acid-induced mitochondrial uncoupling in ... [Diabetologia. 2007] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...17712547

FFA free fatty acids mitochondria insulin resistance type II diabetes inflammation obesity adipose tissue adipocytes

shared by Nathan Goodyear on 22 Dec 11 - No Cached
  • Nathan Goodyear on 22 Dec 11
     
    how increase FFA uncouples mitochondria.  Role in development of insulin resistance and type II diabetes
Nathan Goodyear

Macrophage-secreted factors induce adipocyte inflammation and insulin resistance 10.101... - 0 views

www.sciencedirect.com/...S0006291X06000714

inflammation insulin resistance ATM macrophages obesity overweight weight-loss

shared by Nathan Goodyear on 10 Jan 12 - No Cached
  • Nathan Goodyear on 10 Jan 12
     
    macrophage infiltration of your excess fat results in inflammation and thus insulin resistance.  These are also called ATMs or Adipose Tissue Macrophages.
Nathan Goodyear

Obesity - Inducible Toll-like Receptor and NF-[kappa]B Regulatory Pathway Expression in... - 0 views

www.nature.com/...oby200825a.html

TLR-4 TLR Toll-like receptors NF-kapppB inflammation obesity

shared by Nathan Goodyear on 19 Jan 12 - No Cached
  • TLRs are functionally inducible and associated with downstream NF-B activation and proinflammatory cytokine production.
  • TLRs represent a family of receptors that are critical to the innate immune response against foreign pathogens and microorganisms
  • LPS has been shown to induce proinflammatory chemokine gene expression in differentiated human adipocytes through TLR and NF-B action
  • ...2 more annotations...
  • Stimulation of TLRs initiates intracellular signaling cascades resulting in downstream NF-B and mitogen-activated protein kinase activation and production of proinflammatory chemokines associated with mechanisms of metabolic dysfunction and cardiovascular disease progression.
  • Elevated fatty acids levels associated with obesity activate TLR4 signaling in fat cells and macrophages, and induce insulin resistance in murine models
  • Nathan Goodyear on 19 Jan 12
     
    TLR, especially TLR-4, is directly involved in NF-KappaB activation and release of inflammatory cytokines
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