Skip to main content

Home/ Dr. Goodyear/ Group items tagged Hypertension-and-diabetes

Rss Feed Group items tagged

Filter: All | Bookmarks | Topics Simple Middle
pharmacybiz

Conditions Causing Type 2 Diabetes And High BP : Study - 0 views

www.pharmacy.biz/abetes-and-high-blood-pressure

pharmacy-business Prevalence-of-hypertension-in-type-2-diabetes Type-2-diabetes-and-hypertension-treatment Type-1-diabetes-and-hypertension Hypertension-and-diabetes

shared by pharmacybiz on 17 Jan 22 - No Cached
  • pharmacybiz on 17 Jan 22
     
    A study by scientists in a UK university has shown the scale of the prevalence of a condition that can lead to various cardiometabolic diseases. The study published in the Annals of Internal Medicine journal on Tuesday (January 4) has prompted calls for changes to healthcare policy after researchers revealed, for the first time, the scale of the impact of the condition associated with benign tumours that can lead to type 2 diabetes and high blood pressure. Up to 10 per cent of adults have a benign tumour, or lump, known as an 'adrenal incidentaloma' in their adrenal glands which can be associated with the overproduction of hormones including the stress steroid hormone cortisol that can lead to type 2 diabetes and high blood pressure. Previous small studies suggested that one in three adrenal incidentalomas produce excess cortisol, a condition called mild autonomous cortisol secretion (MACS). An international research team led by the University of Birmingham carried out the largest ever prospective study of over 1,305 patients with adrenal incidentalomas to assess their risk of high blood pressure and type 2 diabetes and their cortisol production by comparing patients with and without MACS.
Nathan Goodyear

Statin use and risk of diabetes mellitus - 0 views

www.ncbi.nlm.nih.gov/...PMC4360430

statin statin therapy diabetes insulin resistance GLUT4 HgbA1c

shared by Nathan Goodyear on 04 Oct 17 - No Cached
  • An increase in new onset diabetes, i.e., 3% in statin arm and 2.4% in placebo arm was reported. This was accompanied by increase in median value of glycated haemoglobin and was one of the earlier studies to report the increase in new onset diabetes in patients on statins
  • Even after adjustment for potential confounders, statin therapy was associated with an increased risk of new-onset diabetes mellitus
  • Authors suggest that statin-induced diabetes mellitus is a medication class effect
  • ...10 more annotations...
  • Another study also reported that as compared to placebo, statin group showed a higher risk of physician reported incident diabetes and it was also observed that risk was higher in women as compared to men
  • Meta-analysis of randomized controlled trials by Sattar et al[25] involving 91140 non-diabetic patients showed that statin therapy was associated with 9% increased risk of incident diabetes
  • A number of studies showed dose dependent association between statin administration and incident diabetes
  • intensive dose of statins was associated with high incidence of new - onset diabetes
  • Treatment with atorvastatin and simvastatin may be associated with an increased risk of new onset diabetes as compared to pravastatin
  • Increased incidence of diabetes was seen with atorvastatin in the Anglo-Scandinavian Cardiac Outcomes Trial
  • Increased insulin resistance secondary to statins was demonstrated in a prospective non randomised study in patients with coronary bypass surgery
  • downregulation of GLUT4
  • Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial--Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial
  • Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial--Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial
  • Nathan Goodyear on 04 Oct 17
     
    Great review article of the increased risk of worsening insulin resistance, glycated hemoglobin, and diabetes risk.  Atorvastatin appears to be the worst culprit.  Mechanism partially through a decrease in GLUT4.
Nathan Goodyear

Hypogonadism and Metabolic Syndrome in Nigerian Male Patients With Both Type 2 Diabetes... - 0 views

www.ncbi.nlm.nih.gov/...PMC3968985

diabetes hypertension blood pressure metabolic syndrome low T Testosterone CVD men male hormone hormones lipids dyslipidemia

shared by Nathan Goodyear on 07 Apr 14 - No Cached
  • Nathan Goodyear on 07 Apr 14
     
    Asian study finds Testosterone is inversely associated with increased central obesity, increased dyslipidemia, and metabolic syndrome in me with new diagnosis of type II diabetes and hypertension.  Men with metabolic syndrome, type II diabetes, and CVD must have appropriate hormone evaluation.
Nathan Goodyear

ScienceDirect - Toxicology and Applied Pharmacology : Arsenic and diabetes and hyperten... - 0 views

www.sciencedirect.com/...S0041008X07000026

Arsenic hypertension HTN HgbA1C diabetes

shared by Nathan Goodyear on 06 Dec 11 - No Cached
  • Nathan Goodyear on 06 Dec 11
     
    long-term exposure to low levels of Arsenic associated with increased hypertension, elevated HgbA1C and many studies Diabetes.
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
  • ...56 more annotations...
  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Metabolic effects of testosterone replacement therapy on hypogonadal men with type 2 di... - 0 views

www.ajandrology.com/article.asp

Testosterone therapy diabetes lipids glucose triglycerides men male hormone hormones

shared by Nathan Goodyear on 17 Jan 14 - No Cached
  • up to 40% of men with T2DM have testosterone deficiency
  • Among diabetic patients, a reduction in sex hormone binding globulin levels induced by insulin resistance leads to a further decline of testosterone levels
  • low bioavailable testosterone concentration was related to decreased lean body mass and muscle strength
  • ...13 more annotations...
  • Testosterone deficiency has a high prevalence in men with T2DM, and it is also associated with impaired insulin sensitivity, increased percentage body fat, central obesity, dyslipidemia, hypertension and cardiovascular diseases (CVD)
  • A meta-analysis of four randomized controlled trials (RCTs) showed that TRT seemed to improve glycemic control as well as fat mass in T2DM subjects with low testosterone levels and sexual dysfunction.
  • testosterone administration could increase muscle mass and strength
  • Insulin stimulates glucose uptake into muscle and adipose tissue via the Glut4 glucose transporter isoform. When insulin activates signaling via the insulin receptor, Glut4 interacts with insulin receptor substrate 1 to initialize intracellular signaling and facilitate glucose transportation into the cell
  • The benefits of TRT on glucose metabolism can mainly be explained by its influence on the insulin signaling pathway
  • Insulin resistance as assessed by, which is calculated from the equation (If*Gf/22.5, where If is fasting insulin and Gf is fasting glucose), was definitely improved by TRT after testosterone administration in three studies
  • Testosterone was observed to elevate the expression levels and stimulate translocation of Glut4 in cultured skeletal muscle cells and to upregulate Glut4 by activating insulin receptor signaling pathways in neonatal rats
  • These effects were inhibited by a dihydrotestosterone (DHT) blocker, indicating that glucose uptake may correlate with conversion of testosterone to DHT and activation of the androgen receptor.
  • TRT reduced triglyceride levels
  • TRT has been reported to have a positive effect in the decrease of total and LDL cholesterol levels and triglycerides in hypogonadal men
  • a recent meta-analysis showed that statins could significantly lower testosterone concentrations.
  • Epidemiological studies have found a negative relationship between testosterone levels and typical cardiovascular risk markers, such as body mass index, waist circumference, visceral adiposity and carotid intima-media thickness.
  • Testosterone treatment was shown to raise hemoglobin, hematocrit and thromboxane, all of which might give rise to CVD
  • Nathan Goodyear on 17 Jan 14
     
    Low Testosterone is a very significant problem in men with type II Diabetes.  Estimated to reach 40%, likely much higher.  They based these estimates only on T levels and sexual symptoms. Testosterone improves glycemic control primarily through Increased transcription and transloction of GLUT4 insulin receptors to the cell surface.  Inflammation reduction is also a mechanism.  Testosteorne lowers Triglycerides in the traditional lipid profile.  Studies are mixed on the other aspects of  lipids.  
Nathan Goodyear

ScienceDirect - Gastroenterology : Obesity, Inflammation, and Insulin Resistance - 0 views

www.sciencedirect.com/...S0016508507005859

inflammation obesity diabetes insulin resistance hypertension

shared by Nathan Goodyear on 21 Dec 11 - No Cached
  • Nathan Goodyear on 21 Dec 11
     
    inflammation contributes to obesity, which increases inflammation; the result are inflammatory disease states: hypertension, diabetes..
Nathan Goodyear

Ascorbic Acid Reduces Blood Pressure and Arterial Stiffness in Type 2 Diabetes | Hypert... - 0 views

hyper.ahajournals.org/...804.long

hypertension blood pressure diabetes vitamin C

shared by Nathan Goodyear on 16 Jan 17 - No Cached
  • Nathan Goodyear on 16 Jan 17
     
    Study finds a nominal dose of vitamin C, 500 mg/day, decreased blood pressure and arterial stiffness in diabetics after only 1 month.  Imagine what you can do with therapeutic levels?
Nathan Goodyear

Testosterone deficiency syndrome and cardiovascular health: An assessment of beliefs, k... - 0 views

www.ncbi.nlm.nih.gov/...PMC3929476

low T Testosterone cardiovascular disease physicians men male hormone hormones

shared by Nathan Goodyear on 03 Mar 14 - No Cached
  • The vast majority (88%) did not screen cardiac patients for TDS.
  • Testosterone deficiency has a prevalence of 7% in the general population, rising to 20% in elderly males
  • Males with CAD have lower testosterone levels than those with normal coronary angiograms of the same age,5 suggesting that the prevalence of testosterone deficiency is much higher in the CAD population
  • ...14 more annotations...
  • Men with hypertension, another established risk factor for CAD, have lower testosterone compared to normotensive men
  • Recent meta-analyses showed that testosterone levels are generally lower among patients with metabolic syndrome, regardless of the various definitions of metabolic syndrome that are used
  • Testosterone (total and bioavailable) and sex-hormone binding globulin (SHBG) are inversely associated with the prevalence of metabolic syndrome in men between the ages of 40 and 80, and this association persists across racial and ethnic backgrounds
  • ower levels of testosterone and SHBG predict a higher incidence of metabolic syndrome.
  • Low testosterone levels have been related to increased insulin resistance and cardiovascular mortality,12 even in the absence of overt type 2 diabetes mellitus.
  • testosterone levels (total and bioavailable) in middle-aged men are inversely correlated with insulin resistance
  • The Massachusetts Male Aging Study (MMAS) demonstrated that low levels of testosterone and SHBG are independent risk factors for the development of type 2 diabetes,
  • Andropausal men (age 58 ± 7 years) have a higher maximal carotid artery intima-media thickness
  • There is an inverse linear correlation between body mass index (BMI) and wait-to-hip ratio with testosterone and insulin-like growth factor-1 levels.
  • Testosterone supplementation for 1 year in hypogonadal men has been shown to cause a significant improvement in body weight, BMI, waist size, lipid profile, and C-reactive protein levels
  • TRT for 3 months in hypogonadal men with type 2 diabetes significantly improved fasting insulin sensitivity, fasting blood glucose and glycated hemoglobin.
  • Testosterone replacement can improve angina symptoms and delay the onset of cardiac ischemia, likely through a coronary vasodilator mechanism
  • ADT is associated with an increased risk of cardiovascular events, including myocardial infarction and cardiovascular mortality.
  • ADT significantly increases fat mass, decreases lean body mass,29,30 increases fasting plasma insulin and decreases insulin sensitivity31 and increases serum cholesterol and triglyceride levels
  • Nathan Goodyear on 03 Mar 14
     
    Startling study on the knowledge of Testosterone and cardiovascular disease in general practitioners and cardiologists in Canada.  Eight-eight percent did not screen patients with cardiovascular disease for low Testosterone.  A whopping 67% of physicians did not know that low T was a risk factor for cardiovascular disease, yet 62% believed Testosterone would increase exercise tolerance. The lack of knowledge displayed by physicians today is staggering and is an indictment of the governing bodies.  This was a survey conducted in Canada so there are obvious limitations to the strength/conclusion of this study.
Nathan Goodyear

Effects of Long-Term Testosterone Therapy on Patients with "Diabesity": Results of Obse... - 0 views

www.hindawi.com/...683515

Testosterone therapy treatment men male hormone hormones diabetes hypogonadism health obese obesity glucose HgbA1c blood pressure hypertension CRP liver enzymes waist circumference low Testosterone low weight low T

shared by Nathan Goodyear on 15 Aug 14 - No Cached
  • Nathan Goodyear on 15 Aug 14
     
    Six years of Testosterone therapy in men with obesity, low T, and type II Diabetes was found to decrease waist circumference, decrease weight, decrease fasting glucose, decrease in HgbA1c and improved systolic/diastolic blood pressure, lipids, CRP, and liver enzymes.
Nathan Goodyear

ScienceDirect - Free Radical Biology and Medicine : Effect of eicosapentaenoic acid and... - 0 views

www.sciencedirect.com/science

DHA EPA omega-3 diabetes high blood pressure oxidative stress

shared by Nathan Goodyear on 15 Feb 11 - No Cached
  • Nathan Goodyear on 15 Feb 11
     
    DHA >EPA in reducing oxidative stress in those with high blood pressure and diabetes; though both effective
Nathan Goodyear

Interaction Between Obesity and the Gut Microbiota: Relevance in Nutrition - 0 views

www.uclouvain.be/...nteraction_between_obesity.pdf

GI gut inflammation dysbiosis obesity insulin resistance IR type II DM diabetes hypertension metabolic endotoxemia

shared by Nathan Goodyear on 08 Mar 12 - No Cached
  • Nathan Goodyear on 08 Mar 12
     
    Gut inflammation resultant from dysbiosis leads to inflammation, obesity, insulin resistance, type II DM, hypertension...
Nathan Goodyear

Dehydroepiandrosterone in the treatment of erectile... [Urol Res. 2001] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...11585284

DHEA ED low libido

shared by Nathan Goodyear on 12 Jun 13 - No Cached
  • Nathan Goodyear on 12 Jun 13
     
    DHEA may be beneficial in those with ED + hypertension and those with organic ED cause.  "Organic" causes like diabetes and neurological problems DHEA provided no benefit.
Nathan Goodyear

Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the met... - 0 views

ajcn.nutrition.org/...899.short

fructose diabetes hypertension metabolic syndrome cardiovascular disease obesity nutrition

shared by Nathan Goodyear on 19 Sep 13 - No Cached
  • Nathan Goodyear on 19 Sep 13
     
    Fructose implicated in just about every chronic disease of aging through obesity.
Nathan Goodyear

http://www.eurjmedres.com/content/pdf/s40001-014-0056-6.pdf - 0 views

www.eurjmedres.com/...s40001-014-0056-6.pdf

Testosterone therapy treatment diet exercise low T low Testosterone low T Diabetes BMI weight HgbA1c hypertension blood pressure men male hormone hormones

shared by Nathan Goodyear on 27 Oct 14 - No Cached
  • Nathan Goodyear on 27 Oct 14
     
    Testosterone therapy in obese men with type II Diabetes and low T improved weight,  lipids, HgbA1c, and blood pressure.  There was more improvement with Leptin than with diet/exercise alone. What is very important is that the control group (diet, exercise, DM meds) had improvement in Testosterone levels, HgbA1c, lipids, BMI, and blood pressure; just not as strong as the treatment arm with Testosterone.
Nathan Goodyear

Prevention of coronary and stroke events with atorvastatin in hypertensive patients who... - 0 views

www.ncbi.nlm.nih.gov/...15765890

statin statin therapy diabetes

shared by Nathan Goodyear on 04 Oct 17 - No Cached
  • Nathan Goodyear on 04 Oct 17
     
    Only abstract available here, but atorvastatin associated with a reduction in cardiovascular events but also associated with increased risk of diabetes.
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

Elderly men over 65 years of age with late-onset hypogonadism benefit as much from test... - 0 views

www.ncbi.nlm.nih.gov/...PMC4392031

low T low Testosterone Testosterone men male hormone hormones late onset hypogonadism hypogonadism

shared by Nathan Goodyear on 21 May 15 - No Cached
  • The benefits of restoring serum testosterone in men with LOH were not significantly different between men older than 65 years of age and younger men. There were no indications that side effects were more severe in elderly men. The effects on prostate and urinary function and hematocrit were within safe margins.
  • obesity, but also impaired general health, are the more common causes of low testosterone in aging men
  • Severe LOH is associated with substantially higher risks of all-cause and cardiovascular mortality,
  • ...30 more annotations...
  • advanced age, obesity, a diagnosis of metabolic syndrome, and poor general health status were predictors of LOH
  • Diabetes mellitus was correlated with hypogonadism in most studies
  • coronary heart disease, hypertension, stroke, and peripheral arterial disease did not predict hypogonadism, they did correlate with the incidence of low testosterone
  • LOH can be defined by the presence of at least three sexual symptoms associated with a total testosterone level of less than 11 nmol/L (3.2 ng/mL) and a free testosterone level of less than 220 pmol/L (64 pg/mL)
    • Nathan Goodyear
      Nathan Goodyear on 27 May 15
       
      the European Male Aging study defined low T as total < 320 ng/dl and free < 64 pg/ml.  
  • Mean weight decreased
  • Waist circumference decreased
  • Total cholesterol decreased
  • Low-density lipoprotein decreased
  • Triglycerides decreased
  • High-density lipoprotein (HDL) increased
  • ratio of total cholesterol to HDL improved
  • Prostate volume increased
  • PSA increased
  • The benefits for men older than 65 years of age were compared with those of younger men, and the improvements in body weight, metabolic factors, psychological functioning, and sexual functioning were of the same magnitude in both age groups
  • weight loss was progressive over the 6-year period, effects of testosterone on lipids and on psychological and sexual functioning reached a plateau after approximately 3 years and these effects were sustained
  • Effects of testosterone on hematopoiesis, on the prostate, and on bladder function were not more severe in older men than in younger men
  • observe a mild increase in prostate volume and serum PSA over time, which is a normal finding in aging men. Maybe somewhat surprising, postvoiding residue and the IPSS did not deteriorate with aging but showed a degree of improvement
  • the severity of the metabolic syndrome is associated with the severity of lower urinary tract symptoms
  • The symptoms of the metabolic syndrome improve upon testosterone treatment and testosterone may thus have a favorable effect on lower urinary tract symptoms
  • it seems reasonable to conclude that the risks of testosterone administration to elderly men are not disproportionately higher in elderly men than in younger men.
  • Despite evidence to the contrary, physicians still harbor a wrongful association between testosterone and the development of prostate pathology (prostate cancer and benign prostate hyperplasia)
  • Not surprisingly, the incidence of prostate cancer was higher in older men; however, it was lower than expected in both groups
  • These observations suggest that the incidence of prostate cancer in patients receiving testosterone therapy, both in the younger and in the older group, was not greater than in the general population not receiving testosterone treatment
  • The historical fear that raising testosterone levels will result in more prostate cancer has been dispelled, particularly by the work of Abraham Morgentaler
  • Higher serum testosterone levels fail to show an increased risk of prostate cancer, and supraphysiological testosterone does not increase prostate volume or PSA in healthy men
  • This apparent paradox is explained by the "saturation model,"
  • Recent studies indicate no increased risk of prostate cancer among men with serum testosterone in the therapeutic range
  • In the present observational study, no cases of major adverse cardiovascular events occurred.
  • the benefits of testosterone therapy are fully achieved only by long-term treatment
  • To achieve maximal benefits, good patient adherence is a prerequisite
  • Nathan Goodyear on 21 May 15
     
    Study finds new difference in Testosterone benefits and/or side effects between men < 65 with low T and men > 65 with low T.
Nathan Goodyear

Increased oxidative stress in obesity: Implications for metabolic syndrome, diabetes, h... - 0 views

www.sciencedirect.com/...S1871403X13000434

oxidative stress obesity hypertension dyslipidemia atherosclerosis cancer metabolic syndrome

shared by Nathan Goodyear on 11 Nov 13 - No Cached
  • Nathan Goodyear on 11 Nov 13
     
    increased oxidative stress, from obesity, linked to most diseases of aging.
Nathan Goodyear

Changes in inflammatory biomarkers acros... [J Gastrointest Surg. 2009] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...19415399

CRP fibrinogen obesity overweight weight-gain diabetes hypertension

shared by Nathan Goodyear on 20 Dec 11 - No Cached
  • Nathan Goodyear on 20 Dec 11
     
    obesity leads to inflammatory marker elevations and associated inflammatory disease states. These results come from the NHANES 1999-2004.
1 - 20 of 22 Next ›
Showing 20▼ items per page