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Nathan Goodyear

http://www.diabetologia-journal.org/files/Narendran.pdf - 0 views

www.diabetologia-journal.org/...Narendran.pdf

exercise inflammation growth hormone GH IGF-1 TNF-alpha IL-6 IL-1beta IL-1Ra interferon-gamma diabetes islet cells

shared by Nathan Goodyear on 28 Oct 14 - No Cached
  • Nathan Goodyear on 28 Oct 14
     
    Exercise is not just for calories out.  Exercise increases growth hormone, IGF-1, glucagon-like peptide 1, IL-6, and IL-1ra.  The effect is to GH increases beta islet cell mass and protects beta cell lines against IL-1beta, Interferon-gamma and TNF-alhpa induced apoptosis.  IL-6 increased production increases GLP-1 and IL-1ra which counters IL-1beta.  Interleukin-1beta induces islet cell apoptosis and thus IL-1ra counters this pro-inflammatory signal.
Nathan Goodyear

Curcumin Extract for Prevention of Type 2 Diabetes - 0 views

care.diabetesjournals.org/...2121.full

diabetes prevention curcumin turmeric

shared by Nathan Goodyear on 07 Aug 13 - No Cached
  • Nathan Goodyear on 07 Aug 13
     
    Curcumin, best taken in form from Turmeric, found to significantly prevent diabetes progression and improve Beta islet cell function.  The dosage used in this 9 month trial was 1500 mg taken in divided dosing.  A major point is that turmeric actually improved pancreatic beta islet cell function and prevented Diabetes.  As "health" care providers our focus should be on prevention of disease.
Nathan Goodyear

JCI - Inflammatory links between obesity and metabolic disease - 0 views

www.jci.org/57132

obesity overweight weight-loss inflammation metabolic disease

shared by Nathan Goodyear on 04 Jan 12 - No Cached
  • metainflammation
  • The chronic nature of obesity produces a tonic low-grade activation of the innate immune system that affects steady-state measures of metabolic homeostasis over time
  • It is clear that inflammation participates in the link between obesity and disease
  • ...25 more annotations...
  • Multiple inflammatory inputs contribute to metabolic dysfunction, including increases in circulating cytokines (10), decreases in protective factors (e.g., adiponectin; ref. 11), and communication between inflammatory and metabolic cells
  • adipose tissue macrophage (ATM)
  • Physiologic enhancement of the M2 pathways (e.g., eosinophil recruitment in parasitic infection) also appears to be capable of reducing metainflammation and improving insulin sensitivity (27).
  • increasing adiposity results in a shift in the inflammatory profile of ATMs as a whole from an M2 state to one in which classical M1 proinflammatory signals predominate (21–23).
  • The M2 activation state is intrinsically linked to the activity of PPARδ and PPARγ
  • well-known regulators of lipid metabolism and mitochondrial activity
  • Independent of obesity, hypothalamic inflammation can impair insulin release from β cells, impair peripheral insulin action, and potentiate hypertension (63–65).
  • inflammation in pancreatic islets can reduce insulin secretion and trigger β cell apoptosis leading to decreased islet mass, critical events in the progression to diabetes (33, 34)
  • Since an estimated excess of 20–30 million macrophages accumulate with each kilogram of excess fat in humans, one could argue that increased adipose tissue mass is de facto a state of increased inflammatory mass
  • JNK, TLR4, ER stress)
  • NAFLD is associated with an increase in M1/Th1 cytokines and quantitative increases in immune cells
  • Upon stimulation by LPS and IFN-γ, macrophages assume a classical proinflammatory activation state (M1) that generates bactericidal or Th1 responses typically associated with obesity
  • DIO, metabolites such as diacylglycerols and ceramides accumulate in the hypothalamus and induce leptin and insulin resistance in the CNS (58, 59)
  • saturated FAs, which activate neuronal JNK and NF-κB signaling pathways with direct effects on leptin and insulin signaling (60)
  • Lipid infusion and a high-fat diet (HFD) activate hypothalamic inflammatory signaling pathways, resulting in increased food intake and nutrient storage (57)
  • Maternal obesity is associated with endotoxemia and ATM accumulation that may affect the developing fetus (73)
  • Placental inflammation is a characteristic of maternal obesity
  • a risk factor for obesity in offspring, and involves inflammatory macrophage infiltration that can alter the maternal-fetal circulation (74
  • Of these PRRs, TLR4 has received the most attention, as this receptor can be activated by free FAs to generate proinflammatory signals and activate NF-κB
  • Nod-like receptor (NLR) family of PRRs
  • ceramides and sphingolipids
  • The adipokine adiponectin has long been recognized to have positive benefits on multiple cell types to promote insulin sensitivity and deactivate proinflammatory pathways.
  • adiponectin stimulates ceramidase activity and modulates the balance between ceramides and sphingosine-1-phosphate
  • Inhibition of ceramide production blocks the ability of saturated FAs to induce insulin resistance (101)
  • NF-κB, obesity also activates JNK in insulin-responsive tissues
  • Nathan Goodyear on 04 Jan 12
     
    must read to see our current knowledge on the link between inflammation and obesity.
Nathan Goodyear

Cytokines in the Progression of Pancreatic β-Cell Dysfunction - 0 views

www.hindawi.com/...515136

inflammation cytokines inflammatory pancreas DM diabetes type II diabetes metabolic endotoxemia

shared by Nathan Goodyear on 15 Jan 13 - No Cached
  • Nathan Goodyear on 15 Jan 13
     
    inflammatory cytokines lead to progressive pancreatic Beta islet cells dysfunction and resultant diabetes.
Nathan Goodyear

Regulation of Cyclooxygenase-2 Expression in Monocytes by Ligation of the Receptor for ... - 0 views

www.jbc.org/...34834.full

COX2 AGE advanced glycation end products RAGE inflammation

shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • Nathan Goodyear on 11 Jun 12
     
    good article on the biochemistry of COX2 in inflammation.  Particularily with AGE and it the receptors RAGE.  COX2 has been shown to decrease insulin secretion through inhibition of islet cell production, but in the presence of disease level inflammation, COX2 can be a part of a very dangerous autocrine/paracrine loop.
Nathan Goodyear

International Journal of Obesity - Antiobesity action of peripheral exenatide (exendin-... - 0 views

www.nature.com/...0803284a.html

exanatide Byetta obesity fatty liver weight loss

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • Systemic exenatide reduces body weight gain in normal, high-fat-fed rodents
  • role in metabolic pathways mediating food intake.
  • the first of which to be identified was an enhancement of glucose-dependent insulin secretion
  • ...5 more annotations...
  • limits glucose appearance via glucose-dependent slowing of gastric emptying
  • suppression of inappropriately elevated postprandial glucagon secretion
  • promote pancreatic -cell proliferation and islet cell neogenesis in both animal and in vitro studies
  • short-term regulator of food intake
  • eceptor agonism in satiety
  • Nathan Goodyear on 06 Apr 11
     
    exanatide helps in obesity and fatty liver treatment
Nathan Goodyear

Gliadin Fragments and a Specific Gliadin 33-mer Peptide Close KATP Channels and Induce ... - 0 views

www.ncbi.nlm.nih.gov/...PMC3681969

Wheat gluten insulin obesity overweight

shared by Nathan Goodyear on 02 Jul 13 - No Cached
  • Nathan Goodyear on 02 Jul 13
     
    Mouse study finds that gluten diet increased weight gain by 20%, partly through increased insulin secretion.
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