Skip to main content

Home/ Dr. Goodyear/ Group items tagged glucagon

Rss Feed Group items tagged

Filter: All | Bookmarks | Topics Simple Middle
Nathan Goodyear

Glucagon-like peptide 1 improves the ability of th... [Diabetes. 1998] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...9703326

glucagon-like peptid-1 insulin glucose control diabetes resistance

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • We concluded that low dosage GLP-1 improves the ability of the beta-cell to secrete insulin in both IGT and NIDDM subjects, but that the ability to sense and respond to subtle changes in plasma glucose is improved in IGT subjects, with only a variable response in NIDDM subjects. Beta-cell dysfunction was improved by GLP-1 infusion, suggesting that early GLP-1 therapy may preserve beta-cell function in subjects with IGT or mild NIDDM.
  • Nathan Goodyear on 06 Apr 11
     
    glucagon-like peptide-1 improves insulin/glucose regulation
Nathan Goodyear

Modulation of the glucagon-like peptide-1 receptor... [J Pharmacol Exp Ther. 2011] - Pu... - 0 views

www.ncbi.nlm.nih.gov/...21075839

flavonoids glucagon-like peptide-1

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • Nathan Goodyear on 06 Apr 11
     
    natural flavonoids act as modulator of glucagon-like peptide-1
Nathan Goodyear

Glucagon Stimulation Testing in Assessing for Adult Growth Hormone Deficiency: Current ... - 0 views

www.ncbi.nlm.nih.gov/...PMC3262627

glucagon stimulation test HGH GH human growth hormone growth hormone

shared by Nathan Goodyear on 04 Nov 14 - No Cached
  • Nathan Goodyear on 04 Nov 14
     
    the Glucagon Stim test is a useful alternative to the ITT for HGH deficiency evaluation.
Nathan Goodyear

Exenatide can reduce glucose independent of islet hormones or gastric emptying - 0 views

ajpendo.physiology.org/...E269.full

glucagon-like peptide-1 exenatide insulin glucose regulation diabetes

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • Nathan Goodyear on 06 Apr 11
     
    glucagon-like peptide-1 useful in glucose/insulin regulation
Nathan Goodyear

Incretin-based therapies: can we achieve glycemic control and cardioprotection? - 0 views

joe.endocrinology-journals.org/...T17.full

incretin incretins GLP-1 glucagon-like peptide 1) glucose homeostasis

shared by Nathan Goodyear on 24 Mar 14 - No Cached
  • Nathan Goodyear on 24 Mar 14
     
    Good discussion on the incretin: (Glucagon-like peptide 1 (GLP-1).
Nathan Goodyear

Extranuclear Actions of the Androgen Receptor Enhance Glucose-Stimulated Insulin Secret... - 0 views

www.cell.com/...S1550-4131(16)30118-8

Testosterone low Testosterone low T hormones male hormones DHT dihydrotestosterone insulin AR androgen receptor Diabetes

shared by Nathan Goodyear on 18 May 16 - No Cached
  • Nathan Goodyear on 18 May 16
     
    only abstract available here. Mouse model finds possible explanation for low Testosterone and diabetes link.  Actually, the link is between the metabolite DHT and the AR. The activity of AR from DHT binding induces beta cell insulin secretion in the presence of glucose.  This is dependent on glucagon-like peptide 1 receptor activation also, which AR activation by DHT does in fact do.
Nathan Goodyear

Therapy in the Early Stage: Incretins - 0 views

care.diabetesjournals.org/...S264.full

incretins glucose diabetes

shared by Nathan Goodyear on 11 Dec 13 - No Cached
  • Increased resistance to insulin action in the skeletal muscle and liver associated with enhanced hepatic glucose output and impaired insulin secretion due to a progressive decline of β-cell function are long-recognized core defects
  • in addition, other mechanisms/organs are involved, augmenting the pathological pathways: adipocytes (altered fat metabolism due to insulin resistance), gastrointestinal tract (incretin deficiency and/or resistance), pancreatic α-cells (hyperglucagonemia and increased hepatic sensitivity to glucagon), kidneys (enhanced glucose reabsorption), and central nervous system (insulin resistance)
  • β-cell failure
    • Nathan Goodyear
      Nathan Goodyear on 11 Dec 13
       
      and studies have shown that a reduction in insulin function will decrease LH production and thus lead to a decrease in Testosterone production in men.
  • ...2 more annotations...
  • Incretins are gut-derived hormones, members of the glucagon superfamily, released in response to nutrient ingestion (mainly glucose and fat)
  • They exert a wide range of effects, including stimulation of pancreatic insulin secretion in a glucose-dependent manner and play an important role in the local gastrointestinal and whole-body physiology
  • Nathan Goodyear on 11 Dec 13
     
    good discussion on incretins and their role in glucose homeostasis. 
Nathan Goodyear

Diagnosing Growth Hormone Deficiency in Adults - 0 views

www.hindawi.com/...972617

HGH GH human growth hormone growth hormone IGF-1

shared by Nathan Goodyear on 04 Nov 14 - No Cached
  • it is clear that serum IGF-1 and or IGFBP-3 can be normal in patients with undisputed GHD
  • Various investigators have reported normal IGF-1 values in 37–70% of GH deficient adults
  • The co-administration of arginine and GHRH (the combined test) is a powerful stimulus for GH production and has gained increasing acceptance as a useful method of diagnosing GHD [34]. This test has been advocated as a suitable alternative to ITT
  • ...12 more annotations...
  • The glucagon stimulation test (GST) is a reliable, safe alternative to the ITT in the diagnosis of GHD
  • It has also been suggested that that even mildly increased BMI (25–30 kg/m2) can result in diminished stimulated GH production in 13% of healthy subjects
  • Obesity, particularly marked obesity, is associated with blunted GH secretion in response to provocative stimuli
  • An intravenous infusion of arginine (0.5 g/kg body weight) together with an intravenous bolus of GHRH (1 mcg/kg body weight) is administered [30]. Serum samples for GH are then obtained every 15–30 minutes for two hours.
  • GH levels are higher during the luteal phase in comparison with the follicular phase of the cycle
  • Corneli et al. have defined BMI-specific cut-off points for diagnosing adult-onset GHD using GHRH + arginine—11.5 ng/mL for those with BMI < 25 kg/m2, 8.0 ng/mL for BMI 25–30 kg/m2, 4.2 ng/mL for those with BMI > 30 kg/m2
  • Oral, in contrast to transdermal oestrogen, lowers IGF-1 levels and is associated with increased GH levels
  • Adequate pituitary replacement with thyroxine and hydrocortisone are needed for optimal GH production
  • one cannot rely on a low IGF-1 to diagnose GHD in women taking oral oestrogen preparations.
  • Numerous GH secretagogues are available with the insulin tolerance test being the gold standard and the glucagon stimulation test or the GHRH + arginine as acceptable alternatives
  • ain et al. found the GST to be at least as good as the ITT in provoking GH secretion
  • the GST is safe, with almost no contraindications, it causes nausea and sometimes vomiting in 15–20% of subjects
  • Nathan Goodyear on 04 Nov 14
     
    Nice, more recent analysis, of HGH testing.
Nathan Goodyear

Effect of Dehydroepiandrosterone Replacement on Insulin Sensitivity and Lipids in Hypoa... - 0 views

diabetes.diabetesjournals.org/...765.long

DHEA hypoadrenia adrenal fatiuge insulin resistance insulin resistance sensitivity

shared by Nathan Goodyear on 03 Aug 14 - No Cached
  • Nathan Goodyear on 03 Aug 14
     
    Study finds 50 mg of DHEA improves insulin sensitivity in Hypoadrenal women.  The authors also found and increase in DHEAS, bioavailable T, androstenedione, and a reduced SHBG, insulin, and glucagon.
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

Chylomicron formation and glucagon-like peptide 1 receptor are involved in activation o... - 0 views

www.jnutbio.com/...abstract

chylomicron inflammation atherosclerosis CAD arteriosclerosis plaque vascular disease

shared by Nathan Goodyear on 01 May 13 - No Cached
  • Nathan Goodyear on 01 May 13
     
    Inflammatory foods coupled with elevated glucose levels and hypertriglyceridemia induces endotoxemia, oxidative damage and immune,inflammatory dysfunction; thus activated chylomicrons
Nathan Goodyear

The expanding role of incretin-based therapies: how much should we expect? - 0 views

joe.endocrinology-journals.org/...E1.full

incretins

shared by Nathan Goodyear on 08 Apr 14 - No Cached
  • The incretins are peptide hormones released from the small intestine during meal absorption that stimulate insulin secretion from pancreatic β-cells and reduce excessive secretion of glucagon by pancreatic α-cells
  • Nathan Goodyear on 08 Apr 14
     
    intro to incretins
Nathan Goodyear

Nutritional Modulation of Insulin Resistance - 0 views

www.hindawi.com/...424780

macronutrient macronutrients nutrition insulin resistance glucose protein carbohydrates metabolism fats

shared by Nathan Goodyear on 21 Oct 13 - No Cached
  • Five branched chain and aromatic amino acids (isoleucine, leucine, valine, tyrosine, and phenylalanine) showed significant associations with future diabetes
  • there is increasing evidence that longer term high-protein intake may have detrimental effects on insulin resistance [68, 117–123], diabetes risk [69], and the risk of developing cardiovascular disease
  • high-protein and the high GI diets significantly increased markers of low-grade inflammation
  • ...5 more annotations...
  • significant and clinically relevant worsening of insulin sensitivity with an isoenergetic plant-based high-protein diet
  • healthy humans that are exposed to amino acid infusions rapidly develop insulin resistance
  • longer term high-protein intake has been shown to result in whole-body insulin resistance [68, 118], associated with upregulation of factors involved in the mammalian target of rapamycin (mTOR)/S6K1 signalling pathway [68], increased stimulation of glucagon and insulin within the endocrine pancreas, high glycogen turnover [118] and stimulation of gluconeogenesis [68, 118].
  • it was recently shown in a large prospective cohort with 10 years followup that consuming 5% of energy from both animal and total protein at the expense of carbohydrates or fat increases diabetes risk by as much as 30% [69]. This reinforces the theory that high-protein diets can have adverse effects on glucose metabolism.
  • Another recent study showed that low-carbohydrate high-protein diets, used on a regular basis and without consideration of the nature of carbohydrates or the source of proteins, are also associated with increased risk of cardiovascular disease [70], thereby indicating a potential link between high-protein Western diets, T2DM, and cardiovascular risk.
  • Nathan Goodyear on 21 Oct 13
     
    macronutrient intake and effect on glucose regulation and thus metabolism.
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

Pharmacokinetics, pharmacodynamics, and safety of exenatide in patients with type 2 dia... - 0 views

www.ajhp.org/...173.short

exenatide byetta diabetes overweight obesity pharmacodynamics pharmacokinetics

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • exenatide dose-dependently reduced postprandial plasma glucose excursion by insulinotropism
  • suppression of plasma glucagon, and slowing of gastric emptying.
  • Nathan Goodyear on 06 Apr 11
     
    exenatide improves insulin/glucose regulation
Nathan Goodyear

Effects of glucagon-like peptide 1 on appetite and body weight: focus on the CNS - 0 views

joe.endocrinology-journals.org/...T1.full

incretins incretin appetite

shared by Nathan Goodyear on 24 Mar 14 - No Cached
  • Nathan Goodyear on 24 Mar 14
     
    To be read article on incretins
Nathan Goodyear

Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk - 0 views

jme.endocrinology-journals.org/...R51.full

metabolic endotoxemia obesity insulin resistance cardiovascular disease LPS inflammation

shared by Nathan Goodyear on 04 Aug 14 - No Cached
  • Weight gain has been associated with a higher gut permeability
  • a high-fat diet promotes LPS absorption
  • higher concentrations of fatty acids impair intestinal barrier integrity
  • ...37 more annotations...
  • The starting point for innate immunity activation is the recognition of conserved structures of bacteria, viruses, and fungal components through pattern-recognition receptors
  • TLRs are PRRs that recognize microbe-associated molecular patterns
  • TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain homologous to the IL1 receptor intracellular domain
  • The major proinflammatory mediators produced by the TLR4 activation in response to endotoxin (LPS) are TNFα, IL1β and IL6, which are also elevated in obese and insulin-resistant patients
  • Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
  • Probiotics, prebiotics, and antibiotic treatment can reduce LPS absorption
  • LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease.
  • In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression.
  • In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
  • the gut microbiota has been recently proposed to be an environmental factor involved in the control of body weight and energy homeostasis by modulating plasma LPS levels
  • dietary fats alone might not be sufficient to cause overweight and obesity, suggesting that a bacterially related factor might be responsible for high-fat diet-induced obesity.
  • This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in Bifidobacterium and Eubacterium spp.
  • n humans, it was also shown that meals with high-fat and high-carbohydrate content (fast-food style western diet) were able to decrease bifidobacteria levels and increase intestinal permeability and LPS concentrations
  • it was demonstrated that, more than the fat amount, its composition was a critical modulator of ME (Laugerette et al. 2012). Very recently, Mani et al. (2013) demonstrated that LPS concentration was increased by a meal rich in saturated fatty acids (SFA), while decreased after a meal rich in n-3 polyunsaturated fatty acids (n-3 PUFA).
  • this effect seems to be due to the fact that some SFA (e.g., lauric and mystiric acids) are part of the lipid-A component of LPS and also to n-3 PUFA's role on reducing LPS potency when substituting SFA in lipid-A
  • these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of LPS-mediated nutritional changes.
  • This suggests a link between gut microbiota, western diet, and obesity and indicates that gut microbiota manipulation can beneficially affect the host's weight and adiposity.
  • endotoxemia was independently associated with energy intake but not fat intake in a multivariate analysis
  • in vitro that endotoxemia activates pro-inflammatory cytokine/chemokine production via NFκB and MAPK signaling in preadipocytes and decreased peroxisome proliferator-activated receptor γ activity and insulin responsiveness in adipocytes.
  • T2DM patients have mean values of LPS that are 76% higher than healthy controls
  • LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both peripheral and hepatic
  • LPSs also seem to induce ROS-mediated apoptosis in pancreatic cells
  • Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression of alcoholic and nonalcoholic fatty liver disease
  • The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted in bile
  • All the subclasses of plasma lipoproteins can bind and neutralize the toxic effects of LPS, both in vitro (Eichbaum et al. 1991) and in vivo (Harris et al. 1990), and this phenomenon seems to be dependent on the number of phospholipids in the lipoprotein surface (Levels et al. 2001). LDL seems to be involved in LPS clearance, but this antiatherogenic effect is outweighed by its proatherogenic features
  • LPS produces hypertriglyceridemia by several mechanisms, depending on LPS concentration. In animal models, low-dose LPS increases hepatic lipoprotein (such as VLDL) synthesis, whereas high-dose LPS decreases lipoprotein catabolism
  • When a dose of LPS similar to that observed in ME was infused in humans, a 2.5-fold increase in endothelial lipase was observed, with consequent reduction in total and HDL. This mechanism may explain low HDL levels in ‘ME’ and other inflammatory conditions such as obesity and metabolic syndrome
  • It is known that the high-fat diet and the ‘ME’ increase intrahepatic triglyceride accumulation, thus synergistically contributing to the development and progression of alcoholic and NAFLD, from the initial stages characterized by intrahepatic triglyceride accumulation up to chronic inflammation (nonalcoholic steatohepatitis), fibrosis, and cirrhosis
  • On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines like TNFα
  • high-fat diet mice presented with ME, which positively and significantly correlated with plasminogen activator inhibitor (PAI-1), IL1, TNFα, STAMP2, NADPHox, MCP-1, and F4/80 (a specific marker of mature macrophages) mRNAs
  • prebiotic administration reduces intestinal permeability to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
  • Cani et al. also found that high-fat diet mice presented with not only ME but also higher levels of inflammatory markers, oxidative stress, and macrophage infiltration markers
  • This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat diet situation
  • high-fat feeding is associated with adipose tissue macrophage infiltration (F4/80-positive cells) and increased levels of chemokine MCP-1, suggesting a strong link between ME, proinflammatory status, oxidative stress, and, lately, increased CV risk
  • LPS has been shown to promote atherosclerosis
  • markers of systemic inflammation such as circulating bacterial endotoxin were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
  • As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory state.
  • Nathan Goodyear on 04 Aug 14
     
    Very nice updated review on Metabolic endotoxemia
Nathan Goodyear

Central Control of Body Weight and Appetite - 0 views

www.ncbi.nlm.nih.gov/...PMC2585760

adipose tissue appetite satiety Gherlin leptin adiponectin insulin glucagon

shared by Nathan Goodyear on 25 Oct 14 - No Cached
  • Nathan Goodyear on 25 Oct 14
     
    great review of adiposity versus satiety signals and the hypothalamus signaling.
Nathan Goodyear

Nutrients | Free Full-Text | Effect of Probiotics on Metabolic Outcomes in Pregnant Wom... - 0 views

www.mdpi.com/...htm

probiotics alternative medicine natural medicine natural therapies diabetes gestational diabetes

shared by Nathan Goodyear on 15 May 17 - No Cached
  • The gut microbial composition is altered during pregnancy
  • probiotic supplements may contribute to the maintenance of bacterial diversity and glucose homeostasis in individuals with metabolic disturbances
  • Assessment of four randomized controlled trials in this review involving 288 pregnant women with GDM found that a 6–8 week probiotic intervention did not improve FBG or LDL-cholesterol levels
  • ...5 more annotations...
  • probiotic supplementation in women with GDM was associated with significant reductions in insulin resistance
  • One proposed method is by the production of short chain fatty acids (SCFAs), generated as a by-product of bacterial fermentation of dietary fibers. SCFAs act as an energy source for intestinal cells and have been found to regulate the production of hormones effecting energy intake and expenditure such as leptin and grehlin
  • Another hypothesized mechanism of SCFA action includes reducing gastrointestinal permeability by upregulating transcription of tight junction proteins, enhancing production of Glucagon-like peptide-2 (GLP-2) which promotes crypt cell proliferation, and reducing inflammation in colonic epithelial cells by increasing PPAR-gamma activation
  • Maintenance of the integrity of the gut barrier minimizes the concentration of lipopolysaccharide (LPS) in circulation
  • LPS is a structural component of gram negative bacterial cell walls, which induces an immune-cell response upon absorption into the human bloodstream, stimulating proinflammatory cytokine production and the onset of insulin resistance and hyperglycemia
  • Nathan Goodyear on 15 May 17
     
    Review (4 studies) found that 6-8 weeks of probiotic therapy of pregnant women with gestational diabetes improved insulin resistance.
  • Open TeleShop on 17 May 17
     
    Hey Dear Check Out Our Online Shopping store in all Over Pakistan.As Seen as On Tv Products Like as Health Beauty,Fitness,Homeware,Kitchenware,And Other Electronic Products in Pakistan Check Out Now| www.openTeleshop.Com
1 - 19 of 19
Showing 20▼ items per page