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Nathan Goodyear

Low-dose naltrexone rescues inflammation and insulin resistance associated with hyperin... - 0 views

pubmed.ncbi.nlm.nih.gov/32943552

insulin resistance low dose naltrexone hyperinsulinemia insulin cancer LDN

shared by Nathan Goodyear on 10 Jan 21 - No Cached
  • Nathan Goodyear on 10 Jan 21
     
    LDN reverses, or rescues, inflammation driven insulin resistance hyperinsulinemia.
Nathan Goodyear

Insulin Resistance Induced by Hyperinsulinemia Coincides with a Persistent Alteration a... - 0 views

journals.plos.org/...article

hyperinsulinemia insulin insulin resistance

shared by Nathan Goodyear on 10 Jan 21 - No Cached
  • Nathan Goodyear on 10 Jan 21
     
    Hyperinsulinemia causes insulin resistance through an attempt to downregulates over signaling.
Nathan Goodyear

Reduction of Chronic Hyperinsulinemia (Insulin Resistance) for the Prevention and Treat... - 0 views

fasting calorie restriction insulin resistance hyperinsulinemia cancer

shared by Nathan Goodyear on 10 Jan 21 - No Cached
  • Nathan Goodyear on 10 Jan 21
     
    Fasting and calorie restriction are a means to attack hyperinsulinemia and insulin resistance.
Nathan Goodyear

Spectrum of metabolic dysfunction in relationship with hyperandrogenemia in obese adole... - 0 views

eje-online.org/...1093.long

PCOS polycystic ovarian syndrome CRP inflammation insulin insulin resistance women female hormone hormones androgens Testosterone hyperandrogenism

shared by Nathan Goodyear on 10 Mar 15 - No Cached
  • subjects with hyperandrogenemic phenotypes displayed the greatest degree of hyperinsulinemia, β-cell function, and chronic inflammation
  • The rise in serum androgens is accompanied by excess insulin secretion, suggesting that insulin directly stimulates ovarian androgen production
  • The degree of hyperinsulinemia does not seem to be directly correlated with the development of HS
  • ...7 more annotations...
  • higher androgen and insulin levels stimulate hair growth
  • genetic and epigenetic changes may be involved in the pathogenesis of PCOS
  • HA has been identified as an important risk factor for MS and dyslipidemias in premenopausal women and adolescents
  • In our study, HA was found to be an independent risk factor for MS as previously reported by Coviello et al.
  • obesity and HA, and not insulin resistance, are the major determinants of chronic inflammation and risk of atherosclerosis in adolescents with PCOS
  • use of an inflammation marker may help identify high-risk females with PCOS
  • hyperandrogenemic PCOS phenotypes have greatest degree of hyperinsulinemia, insulin resistance, and inflammation
  • Nathan Goodyear on 10 Mar 15
     
    Elevated androgens are associated increasing insulin, insulin resistance, and inflammation (as measured by CRP).
Nathan Goodyear

'Metabolic syndrome' in the brain: deficiency in omega-3 fatty acid exacerbates dysfunc... - 0 views

jp.physoc.org/2485

HFCS high-fructose corn syrup n-3 omega-3 metabolic syndrome brain insulin MetS

shared by Nathan Goodyear on 16 May 12 - No Cached
  • Nathan Goodyear on 16 May 12
     
    diets with high high-fructose corn syrup and low omega-3 shown to slow cognitive processing in rat model.  This is basically, metabolic syndrome of the brain, as it is the result of hyperinsulinemia.
Nathan Goodyear

Hyperinsulinemia provokes synchronous increases in... [Arch Neurol. 2005] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...16216936

hyperinsulinemia neurodegenerative disease Alzheimer's inflammation

shared by Nathan Goodyear on 17 Mar 11 - No Cached
  • Nathan Goodyear on 17 Mar 11
     
    elevated insulin increases brain inflammation and thus increases alzheimer's disease risk
Nathan Goodyear

http://annonc.oxfordjournals.org/content/12/11/1533.full.pdf#page=1&view=FitH - 0 views

annonc.oxfordjournals.org/...1533.full.pdf

cancer carbohydrates insulin breast cancer diet nutrition glycemic index glycemic load IGF-1 SHBG

shared by Nathan Goodyear on 09 Dec 14 - No Cached
  • Nathan Goodyear on 09 Dec 14
     
    Study finds link between higher glycemic index and glycemic load with increased breast cancer risk.   The proposed mechanisms are: hyperinsulinemia and its affinity for IGF-1 receptor resulting in a + growth signal.  Increased IGF-1 via the same mechanism. Insulin and IGF-1 have negative regulation effects on SHBG. This all makes sense as insulin receptors are highly expressed on cancer cells.
Nathan Goodyear

Patients with metabolic syndrome and widespread high grade prostati... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...23273912

prostate cancer cancer men male hormone hormones metabolic syndrome low T low Testosterone

shared by Nathan Goodyear on 02 Feb 15 - No Cached
  • Nathan Goodyear on 02 Feb 15
     
    Metabolic Syndrome increases the risk of prostate cancer in men.  No surprise here as low T and hyperinsulinemia are both implicated in development of high grade prostate cancer.
Nathan Goodyear

Hyperinsulinemia enhances transcriptional activity of nuclear factor-kappaB induced by ... - 0 views

pubmed.ncbi.nlm.nih.gov/11055977

insulin NF-kappaB cancer inflammation hyperinsulinemia

shared by Nathan Goodyear on 19 Dec 20 - No Cached
  • Nathan Goodyear on 19 Dec 20
     
    insulin potentiates NF-kappaB-dependent transcriptional activity induced by hyperglycemia
Nathan Goodyear

Is central obesity, hyperinsulinemia and dyslipidemia associated with high-grade prosta... - 0 views

www.ncbi.nlm.nih.gov/...PMC3034056

inflammation prostate cancer CA high-grade IR insulin resistance dyslipidemia obesity overweight weight-gain men

shared by Nathan Goodyear on 11 Feb 12 - No Cached
  • Nathan Goodyear on 11 Feb 12
     
    No surprise that insulin resistance, dyslipidemia, and obesity are associated with high-grade prostate cancer.  It's called inflammation.
Nathan Goodyear

Hypoadiponectinemia in Obesity and Type 2 Diabetes: Close Association with Insulin Resi... - 0 views

jcem.endojournals.org/...1930.short

obesity diabetes type II 2 insulin resistance IR adiponectin

shared by Nathan Goodyear on 17 Mar 12 - No Cached
  • Nathan Goodyear on 17 Mar 12
     
    obesity and type II diabetes found to be associated with low adiponectin and elevated insulin as found in insulin resistance.  This study revealed the inverse relationship of adiponectin and insulin resistance.  The interesting thing is that inflammation causes insulin resistance.  Here you can see the inflammation-insulin resistance-low adiponectin-obesity-diabetes link.
Nathan Goodyear

Insulin resistance and endothelial function are improved after folate and vitamin B12 t... - 0 views

eje-online.org/...483.full.pdf+html

metabolic syndrome vitamin B12 vitamins Folic acid IR insulin resistance endothelial dysfunction homocysteine

shared by Nathan Goodyear on 25 Jul 12 - No Cached
  • Nathan Goodyear on 25 Jul 12
     
    Vitamin B12 and Folic acid improves insulin resistance, endothelial dysfunction, and reduces homocysteine levels by 28% in those with metabolic syndrome.
Nathan Goodyear

Lowered testosterone in male obesity: Mechanisms, morbidity and management Tang Fui MN,... - 0 views

www.ajandrology.com/article.asp

Testosterone male obesity overweight men hormone hormones low T Low T

shared by Nathan Goodyear on 15 Jan 14 - No Cached
  • The number of overweight people is expected to increase from 937 million in 2005 to 1.35 billion in 2030
  • Similarly the number of obese people is projected to increase from 396 million in 2005 to 573 million in 2030
  • By 2030, China alone is predicted to have more overweight men and women than the traditional market economies combined
  • ...37 more annotations...
  • diacylglycerol O-acyltransferase 2 (DGAT2), mechanistically implicated in this differential storage, [10] is regulated by dihydrotestosterone, [11] suggesting a potential role for androgens to influence the genetic predisposition to either the MHO or MONW phenotype.
  • bariatric surgery achieves 10%-30% long-term weight loss in controlled studies
  • The fact that obese men have lower testosterone compared to lean men has been recognized for more than 30 years
  • Reductions in testosterone levels correlate with the severity of obesity and men
  • epidemiological data suggest that the single most powerful predictor of low testosterone is obesity, and that obesity is a major contributor of the age-associated decline in testosterone levels.
  • healthy ageing by itself is uncommonly associated with marked reductions in testosterone levels
  • obesity blunts this LH rise, obesity leads to hypothalamic-pituitary suppression irrespective of age which cannot be compensated for by physiological mechanisms
  • Reductions in total testosterone levels are largely a consequence of reductions in sex hormone binding globulin (SHBG) due to obesity-associated hyperinsulinemia
  • although controversial, measurement of free testosterone levels may provide a more accurate assessment of androgen status than the (usually preferred) measurement of total testosterone in situations where SHBG levels are outside the reference range
  • SHBG increases with age
  • marked obesity however is associated with an unequivocal reduction of free testosterone levels, where LH and follicle stimulating hormone (FSH) levels are usually low or inappropriately normal, suggesting that the dominant suppression occurs at the hypothalamic-pituitary level
  • adipose tissue, especially when in the inflamed, insulin-resistant state, expresses aromatase which converts testosterone to estradiol (E 2 ). Adipose E 2 in turn may feedback negatively to decrease pituitary gonadotropin secretion
  • diabetic obesity is associated with decreases in circulatory E 2
  • In addition to E 2 , increased visceral fat also releases increased amounts of pro-inflammatory cytokines, insulin and leptin; all of which may inhibit the activity of the HPT axis at multiple levels
  • In the prospective Massachusetts Male Aging Study (MMAS), moving from a non-obese to an obese state resulted in a decline of testosterone levels
  • weight loss, whether by diet or surgery, increases testosterone levels proportional to the amount of weight lost
  • fat is androgen-responsive
  • low testosterone may augment the effects of a hypercaloric diet
  • In human male ex vivo adipose tissue, testosterone decreased adipocyte differentiation by 50%.
  • Testosterone enhances catecholamine-induced lipolysis in vitro and reduces lipoprotein lipase activity and triglyceride uptake in human abdominal adipose tissue in vivo
  • in men with prostate cancer receiving 12 months of androgen deprivation therapy, fat mass increased by 3.4 kg and abdominal VAT by 22%, with the majority of these changes established within 6 months
  • severe sex steroid deficiency can increase fat mass rapidly
  • bidirectional relationship between testosterone and obesity
  • increasing body fat suppresses the HPT axis by multiple mechanisms [30] via increased secretion of pro-inflammatory cytokines, insulin resistance and diabetes; [19],[44] while on the other hand low testosterone promotes further accumulation of total and visceral fat mass, thereby exacerbating the gonadotropin inhibition
  • androgens may play a more significant role in VAT than SAT
  • men undergoing androgen depletion for prostate cancer show more marked increases in visceral compared to subcutaneous fat following treatment
    • Nathan Goodyear
      Nathan Goodyear on 16 Jan 14
       
      Interesting: low T increases VAT, yet T therapy does not reduce VAT, yet T therapy reduces SAT.
  • irisin, derived from muscle, induces brown fat-like properties in rodent white fat
  • androgens can act via the PPARg-pathway [37] which is implicated in the differentiation of precursor fat cells to the energy-consuming phenotype
  • low testosterone may compound the effect of increasing fat mass by making it more difficult for obese men to lose weight via exercise
  • pro-inflammatory cytokines released by adipose tissue may contribute to loss of muscle mass and function, leading to inactivity and further weight gain in a vicious cycle
  • Sarcopenic obesity, a phenotype recapitulated in men receiving ADT for prostate cancer, [55] may not only be associated with functional limitations, but also aggravate the metabolic risks of obesity;
  • observational evidence associating higher endogenous testosterone with reduced loss of muscle mass and crude measures of muscle function in men losing weight
  • genuine reactivation of the HPT axis in obese men requires more substantial weight-loss
  • A number of intervention studies have confirmed that both diet- and surgically-induced weight losses are associated with increased testosterone, with the rise in testosterone generally proportional to the amount of weight lost
  • men, regardless of obesity level, can benefit from the effect of weight loss.
  • inconsistent effect of testosterone on VAT
  • Nathan Goodyear on 15 Jan 14
     
    to be read
Nathan Goodyear

Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslip... - 0 views

www.nutritionandmetabolism.com/...5

fructose metabolic syndrome metabolic syndrome insulin resistance obesity nutrition metabolism

shared by Nathan Goodyear on 16 Sep 13 - Cached
  • For thousands of years humans consumed fructose amounting to 16–20 grams per day
  • daily consumptions amounting to 85–100 grams of fructose per day
  • Of key importance is the ability of fructose to by-pass the main regulatory step of glycolysis, the conversion of glucose-6-phosphate to fructose 1,6-bisphosphate, controlled by phosphofructokinase
  • ...29 more annotations...
  • Thus, while glucose metabolism is negatively regulated by phosphofructokinase, fructose can continuously enter the glycolytic pathway. Therefore, fructose can uncontrollably produce glucose, glycogen, lactate, and pyruvate, providing both the glycerol and acyl portions of acyl-glycerol molecules. These particular substrates, and the resultant excess energy flux due to unregulated fructose metabolism, will promote the over-production of TG (reviewed in [53]).
  • Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects
  • reduction in circulating leptin both in the short and long-term as well as a 30% reduction in ghrelin (an orexigenic gastroenteric hormone) in the fructose group compared to the glucose group.
  • A prolonged elevation of TG was also seen in the high fructose subjects
  • Both fat and fructose consumption usually results in low leptin concentrations which, in turn, leads to overeating in populations consuming energy from these particular macronutrients
  • Chronic fructose consumption reduces adiponectin responses, contributing to insulin resistance
  • A definite relationship has also been found between metabolic syndrome and hyperhomocysteinemia
  • the liver takes up dietary fructose rapidly where it can be converted to glycerol-3-phosphate. This substrate favours esterification of unbound FFA to form the TG
  • Fructose stimulates TG production, but impairs removal, creating the known dyslipidemic profile
  • the effects of fructose in promoting TG synthesis are independent of insulinemia
  • Although fructose does not appear to acutely increase insulin levels, chronic exposure seems to indirectly cause hyperinsulinemia and obesity through other mechanisms. One proposed mechanism involves GLUT5
  • If FFA are not removed from tissues, as occurs in fructose fed insulin resistant models, there is an increased energy and FFA flux that leads to the increased secretion of TG
  • In these scenarios, where there is excess hepatic fatty acid uptake, synthesis and secretion, 'input' of fats in the liver exceed 'outputs', and hepatic steatosis occurs
  • Carbohydrate induced hypertriglycerolemia results from a combination of both TG overproduction, and inadequate TG clearance
  • fructose-induced metabolic dyslipidemia is usually accompanied by whole body insulin resistance [100] and reduced hepatic insulin sensitivity
  • Excess VLDL secretion has been shown to deliver increased fatty acids and TG to muscle and other tissues, further inducing insulin resistance
  • the metabolic effects of fructose occur through rapid utilization in the liver due to the bypassing of the regulatory phosphofructokinase step in glycolysis. This in turn causes activation of pyruvate dehydrogenase, and subsequent modifications favoring esterification of fatty acids, again leading to increased VLDL secretion
  • High fructose diets can have a hypertriglyceridemic and pro-oxidant effect
  • Oxidative stress has often been implicated in the pathology of insulin resistance induced by fructose feeding
  • Administration of alpha-lipoic acid (LA) has been shown to prevent these changes, and improve insulin sensitivity
  • LA treatment also prevents several deleterious effects of fructose feeding: the increases in cholesterol, TG, activity of lipogenic enzymes, and VLDL secretion
  • Fructose has also been implicated in reducing PPARα levels
  • PPARα is a ligand activated nuclear hormone receptor that is responsible for inducing mitochondrial and peroxisomal β-oxidation
  • decreased PPARα expression can result in reduced oxidation, leading to cellular lipid accumulation
  • fructose diets altered the structure and function of VLDL particles causing and increase in the TG: protein ratio
  • LDL particle size has been found to be inversely related to TG concentration
  • therefore the higher TG results in a smaller, denser, more atherogenic LDL particle, which contributes to the morbidity of the metabolic disorders associated with insulin resistance
  • High fructose, which stimulates VLDL secretion, may initiate the cycle that results in metabolic syndrome long before type 2 diabetes and obesity develop
  • A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, disturbs normal hepatic carbohydrate metabolism leading to two major consequences (Figure 2): perturbations in glucose metabolism and glucose uptake pathways, and a significantly enhanced rate of de novo lipogenesis and TG synthesis, driven by the high flux of glycerol and acyl portions of TG molecules coming from fructose catabolism
  • Nathan Goodyear on 16 Sep 13
     
    Fructose and metabolic syndrome.  Good discussion of the impact of high fructose intake and metabolic dysfunction.  This study also does a great job of highlighting the historical change of fructose intake.
Nathan Goodyear

Association between hyperinsulinemia and endogeno... [Metabolism. 2002] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...11833055

metabolic syndrome insulin resistance CVD cardiovascular disease menopause perimenopause Testosterone women

shared by Nathan Goodyear on 30 Aug 13 - No Cached
  • Nathan Goodyear on 30 Aug 13
     
    Increasing androgen levels associated with perimenopause/menopause transition.  This is associated with increasing insulin resistance.
Nathan Goodyear

Fructose, weight gain, and the insulin resistance syndrome - 0 views

www.ajcn.org/...911.abstract

overweight weight gain insulin fructose leptin resistance

shared by Nathan Goodyear on 26 May 11 - No Cached
  • he combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae
  • fructose, compared with glucose, is preferentially metabolized to lipid in the liver
  • Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models
  • Nathan Goodyear on 26 May 11
     
    Fructose increase in American diets parallels obesity rise in Americans;  Physiologic mechanism of fructose contribution to obesity discussed
Nathan Goodyear

Association of nonalcoholic fatty liver disease with insulin resistance - 0 views

www.amjmed.com/...abstract

fatty liver and insulin resistance

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • Nonalcoholic fatty liver disease is associated with insulin resistance and hyperinsulinemia
  • educe insulin sensitivity and increase serum triglyceride levels may be responsible for its development.
  • Genetic factors that
  • Nathan Goodyear on 06 Apr 11
     
    Insulin resistance and fatty liver
Nathan Goodyear

Inborn-like errors of metabolism are determinants of breast cancer risk, clinical respo... - 0 views

www.ncbi.nlm.nih.gov/...PMC6114970

cancer metabolism breast cancer glutamine glutamate aspartate oncogenes

shared by Nathan Goodyear on 24 Sep 18 - No Cached
  • We now recognize that human cancers evolve in an environment of metabolic stress. Rapidly proliferating tumor cells deprived of adequate oxygen, nutrients, hormones and growth factors up-regulate pathways that address these deficiencies to overcome hypoxia (HIF), vascular insufficiency (VEGF), growth factor deprivation (EGFR, HER2) and the loss of hormonal support (ER, PR, AR) all to enhance survival and proliferation
  • RAS, PI3K, TP53 and MYC
  • The results suggest that breast cancer could be preceded by systemic subclinical disturbances in glucose-insulin homeostasis characterized by mild, likely asymptomatic, IEM-like biochemical changes
  • ...16 more annotations...
  • The process would include variable periods of hyperinsulinemia with the consequent systemic MYC activation of glycolysis, glutaminolysis, structural lipidogenesis and further exacerbation of hypoglycemia, the result of MYC's known role as an inhibitor of liver gluconeogenesis
  • The metabolic changes we describe in breast cancer arise in concert with IEM-like changes in oxidative phosphorylation as detected by increased values of the ratio lactate/pyruvate (Supplementary Table 2A, 2B) characteristic of Ox/Phos deficiency [25]. In our study, 76% (70/92) of the European breast cancer patients had lactate/pyruvate ratios values higher than the normal value of 25.8
  • four-fold higher frequency of cancer (including breast) in patients with energy metabolism disorders
  • growing recognition that cancer cells differ from their normal counterparts in their use of nutrients, synthesis of biomolecules and generation of energy
  • glutamine concentrations in the cancer patients were reduced to nearly 1/8 of the levels observed in the normal population
  • blood concentrations of aspartate (p = 1.7e-67, FDR = 8.3e-67) (Figure ​(Figure1E)1E) and glutamate (p = 6.4e-96, FDR = 6.2e-95) (Figure ​(Figure1F)1F) were nearly 10 fold higher than the normal ranges of 0–5 μM/L and 40 μM/L, respectively
  • glutamine consumption associated with parallel increases in glutamate and aspartate (Figure ​(Figure1A1A red arrows) is considered a hallmark of MYC-driven “glutaminolysis”
  • Gln/Glu ratio inversely correlates with i- late stage metabolic syndrome and with ii- increased chance of death
  • changes in glutamine consumption, reflected by the Gln/Glu ratio could provide a metabolic link between breast cancer initiation and diabetes, reflective of a systemic metabolic reprogramming from glucose to glutamine as the preferred source of precursors for biosynthetic reactions and cellular energy
  • lower Gln/Glu ratios inversely correlated with insulin resistance and the risk of diabetes
  • the metabolic dependencies of cancer characterized by excessive glycolysis, glutaminolysis and malignant lipidogenesis, previously considered a consequence of local tumor DNA aberration [23] could, instead, represent a systemic biochemical aberration that predates and very likely promotes tumorigenesis
  • these metabolic disturbances would be expected to remain extant after therapeutic interventions
  • accumulation of very long chain acylcarnitines such as C14:1-OH (p = 0.0, FDR = 0.0), C16 (p = 0.0, FDR = 0.0), C18 (p = 0.0, FDR = 0.0) and C18:1 (p = 1.73e-322, FDR = 1.16-321) and lipids containing VLCFA (lysoPC a C28:0) (p = 1.14-e95, FDR = 1.65e-95) in the blood of breast and colon cancer patients
  • Among the most powerful metabolic equations for MYC-activation is that which links the widely used MYC-driven desaturation marker ratio of SFA/MUFA to the MYC glutaminolysis-associated ratio of (Asp/Gln)
  • liver dysfunction shares many features with both IEM and cancer suggesting a role for hepatic dysfunction in carcinogenesis
  • cancer “conscripts” the human genome to meet its needs under conditions of systemic metabolic stress
  • Nathan Goodyear on 24 Sep 18
     
    Breast cancer is a metabolic disease.  Now, where have I heard that cancer is a metabolic disease?
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