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Nathan Goodyear

Obesity, adipocytokines, and cancer - 0 views

dl-web.dropbox.com/...ytokines%2C%20and%20cancer.pdf

adipocytokines leptin adiponectin inflammation cancer insulin resistance IR obesity

shared by Nathan Goodyear on 12 Jan 12 - No Cached
  • Nathan Goodyear on 12 Jan 12
     
    adipocytokines, such as leptin and adiponectin, impact much more than insulin resistance and obesity. Leptin and adiponectin play some role in the development of certain cancers. Bringing together the common thread of inflammation
Nathan Goodyear

Metabolic influences on neuroendocrine regulation of reproduction - 0 views

www.ncbi.nlm.nih.gov/...PMC3898855

metabolism metabolic regulation reproduction Leptin Ghrelin Insulin Kisspeptin GNRH

shared by Nathan Goodyear on 17 Feb 14 - No Cached
  • Energy storage occurs mainly at the level of white adipose tissue, where adipocytes secrete the anorexigenic adipokine leptin
  • humans and laboratory animals with leptin or insulin deficiency or resistance and/or increased ghrelin levels exhibit delayed or absent puberty and frequently display hypogonadotropic hypogonadism, which prevents fertility
  • Ghrelin suppresses pulsatile gonadotropin-releasing hormone (GnRH) release [14,15], thus serving as a signal to suppress reproduction in times of famine
  • ...4 more annotations...
  • Neuropeptides derived from POMC/CART neurons exert a potent anorectic action, thus decreasing food intake and body weight
  • AgRP and NPY have the opposite (orexigenic) effect, inducing food intake.
  • GnRH neurons have been shown to express insulin receptor mRNA and protein [27] and are activated by insulin
  • Kisspeptins (encoded by KISS1) have been identified in the last decade as the most potent secretagogues of GnRH release.
  • Nathan Goodyear on 17 Feb 14
     
    Good, although brief, discussion of the interaction between metabolism and hormones.  Kisspeptin is a GNRH secreatagogue "upstream".   Insulin, Leptin, and Gherlin can inhibit GNRH through resistance and low levels.  Probably a U shaped graph of optimal activity.
Nathan Goodyear

Exercise protects against high-fat diet-induced hypothalamic inflammation. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...22483785

exercise inflammation insulin resistance leptin resistance leptin insulin microglia diet nutrition

shared by Nathan Goodyear on 05 Jun 16 - No Cached
  • Nathan Goodyear on 05 Jun 16
     
    regular treadmill exercise reduced hypothalamic inflammation, improved insulin resistance, improved leptin resistance, improved glucose tolerance, and decreased microglia activation in high-fat animal model.
Nathan Goodyear

Curcumin inhibits hepatic protein-tyrosine phosphatase 1B and prevents hypertriglycerid... - 0 views

www.ncbi.nlm.nih.gov/...20222050

curcumin polyphenols leptin obesity leptin resistance insulin insulin resistance fructose diet

shared by Nathan Goodyear on 05 Jun 16 - No Cached
  • Nathan Goodyear on 05 Jun 16
     
    curcumin found to reduce leptin resistance and insulin resistance in fructose-induced hypertriglyceridiemia in rat model.
Nathan Goodyear

Testosterone and glucose metabolism in men: current concepts and controversies - 0 views

joe.endocrinology-journals.org/...R37.full

Low T Testosterone metabolic syndrome MetS Diabetes men male glucose hormone hormones g

shared by Nathan Goodyear on 04 Feb 14 - No Cached
  • Around 50% of ageing, obese men presenting to the diabetes clinic have lowered testosterone levels relative to reference ranges based on healthy young men
  • The absence of high-level evidence in this area is illustrated by the Endocrine Society testosterone therapy in men with androgen deficiency clinical practice guidelines (Bhasin et al. 2010), which are appropriate for, but not specific to men with metabolic disorders. All 32 recommendations made in these guidelines are based on either very low or low quality evidence.
  • A key concept relates to making a distinction between replacement and pharmacological testosterone therapy
  • ...59 more annotations...
  • The presence of symptoms was more closely linked to increasing age than to testosterone levels
  • Findings similar to type 2 diabetes were reported for men with the metabolic syndrome, which were associated with reductions in total testosterone of −2.2 nmol/l (95% CI −2.41 to 1.94) and in free testosterone
  • low testosterone is more predictive of the metabolic syndrome in lean men
  • Cross-sectional studies uniformly show that 30–50% of men with type 2 diabetes have lowered circulating testosterone levels, relative to references based on healthy young men
  • In a recent cross-sectional study of 240 middle-aged men (mean age 54 years) with either type 2 diabetes, type 1 diabetes or without diabetes (Ng Tang Fui et al. 2013b), increasing BMI and age were dominant drivers of low total and free testosterone respectively.
  • both diabetes and the metabolic syndrome are associated with a modest reduction in testosterone, in magnitude comparable with the effect of 10 years of ageing
  • In a cross-sectional study of 490 men with type 2 diabetes, there was a strong independent association of low testosterone with anaemia
  • In men, low testosterone is a marker of poor health, and may improve our ability to predict risk
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      probably the most important point made in this article
  • low testosterone identifies men with an adverse metabolic phenotype
  • Diabetic men with low testosterone are significantly more likely to be obese or insulin resistant
  • increased inflammation, evidenced by higher CRP levels
  • Bioavailable but not free testosterone was independently predictive of mortality
  • It remains possible that low testosterone is a consequence of insulin resistance, or simply a biomarker, co-existing because of in-common risk factors.
  • In prospective studies, reviewed in detail elsewhere (Grossmann et al. 2010) the inverse association of low testosterone with metabolic syndrome or diabetes is less consistent for free testosterone compared with total testosterone
  • In a study from the Framingham cohort, SHBG but not testosterone was prospectively and independently associated with incident metabolic syndrome
  • low SHBG (Ding et al. 2009) but not testosterone (Haring et al. 2013) with an increased risk of future diabetes
  • In cross-sectional studies of men with (Grossmann et al. 2008) and without (Bonnet et al. 2013) diabetes, SHBG but not testosterone was inversely associated with worse glycaemic control
  • SHBG may have biological actions beyond serving as a carrier protein for and regulator of circulating sex steroids
  • In men with diabetes, free testosterone, if measured by gold standard equilibrium dialysis (Dhindsa et al. 2004), is reduced
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      expensive, laborious process filled with variables
  • Low free testosterone remains inversely associated with insulin resistance, independent of SHBG (Grossmann et al. 2008). This suggests that the low testosterone–dysglycaemia association is not solely a consequence of low SHBG.
  • Experimental evidence reviewed below suggests that visceral adipose tissue is an important intermediate (rather than a confounder) in the inverse association of testosterone with insulin resistance and metabolic disorders.
  • testosterone promotes the commitment of pluripotent stem cells into the myogenic lineage and inhibits their differentiation into adipocytes
  • testosterone regulates the metabolic functions of mature adipocytes (Xu et al. 1991, Marin et al. 1995) and myocytes (Pitteloud et al. 2005) in ways that reduce insulin resistance.
  • Pre-clinical evidence (reviewed in Rao et al. (2013)) suggests that at the cellular level, testosterone may improve glucose metabolism by modulating the expression of the glucose-transported Glut4 and the insulin receptor, as well as by regulating key enzymes involved in glycolysis.
  • More recently testosterone has been shown to protect murine pancreatic β cells against glucotoxicity-induced apoptosis
  • Interestingly, a reciprocal feedback also appears to exist, given that not only chronic (Cameron et al. 1990, Allan 2013) but also, as shown more recently (Iranmanesh et al. 2012, Caronia et al. 2013), acute hyperglycaemia can lower testosterone levels.
  • There is also evidence that testosterone regulates insulin sensitivity directly and acutely
  • In men with prostate cancer commencing androgen deprivation therapy, both total as well as, although not in all studies (Smith 2004), visceral fat mass increases (Hamilton et al. 2011) within 3 months
  • More prolonged (>12 months) androgen deprivation therapy has been associated with increased risk of diabetes in several large observational registry studies
  • Testosterone has also been shown to reduce the concentration of pro-inflammatory cytokines in some, but not all studies, reviewed recently in Kelly & Jones (2013). It is not know whether this effect is independent of testosterone-induced changes in body composition.
  • the observations discussed in this section suggest that it is the decrease in testosterone that causes insulin resistance and diabetes. One important caveat remains: the strongest evidence that low testosterone is the cause rather than consequence of insulin resistance comes from men with prostate cancer (Grossmann & Zajac 2011a) or biochemical castration, and from mice lacking the androgen receptor.
  • Several large prospective studies have shown that weight gain or development of type 2 diabetes is major drivers of the age-related decline in testosterone levels
  • there is increasing evidence that healthy ageing by itself is generally not associated with marked reductions in testosterone
  • Circulating testosterone, on an average 30%, is lower in obese compared with lean men
  • increased visceral fat is an important component in the association of low testosterone and insulin resistance
  • The vast majority of men with metabolic disorders have functional gonadal axis suppression with modest reductions in testosterone levels
  • obesity is a dominant risk factor
  • men with Klinefelter syndrome have an increased risk of metabolic disorders. Interestingly, greater body fat mass is already present before puberty
  • Only 5% of men with type 2 diabetes have elevated LH levels
  • inhibition of the gonadal axis predominantly takes place in the hypothalamus, especially with more severe obesity
  • Metabolic factors, such as leptin, insulin (via deficiency or resistance) and ghrelin are believed to act at the ventromedial and arcuate nuclei of the hypothalamus to inhibit gonadotropin-releasing hormone (GNRH) secretion from GNRH neurons situated in the preoptic area
  • kisspeptin has emerged as one of the most potent secretagogues of GNRH release
  • hypothesis that obesity-mediated inhibition of kisspeptin signalling contributes to the suppression of the HPT axis, infusion of a bioactive kisspeptin fragment has been recently shown to robustly increase LH pulsatility, LH levels and circulating testosterone in hypotestosteronaemic men with type 2 diabetes
  • A smaller study with a similar experimental design found that acute testosterone withdrawal reduced insulin sensitivity independent of body weight, whereas oestradiol withdrawal had no effects
  • suppression of the diabesity-associated HPT axis is functional, and may hence be reversible
  • Obesity and dysglycaemia and associated comorbidities such as obstructive sleep apnoea (Hoyos et al. 2012b) are important contributors to the suppression of the HPT axis
  • weight gain and development of diabetes accelerate the age-related decline in testosterone
  • Modifiable risk factors such as obesity and co-morbidities are more strongly associated with a decline in circulating testosterone levels than age alone
  • 55% of symptomatic androgen deficiency reverted to a normal testosterone or an asymptomatic state after 8-year follow-up, suggesting that androgen deficiency is not a stable state
  • Weight loss can reactivate the hypothalamic–pituitary–testicular axis
  • Leptin treatment resolves hypogonadism in leptin-deficient men
  • The hypothalamic–pituitary–testicular axis remains responsive to treatment with aromatase inhibitors or selective oestrogen receptor modulators in obese men
  • Kisspeptin treatment increases LH secretion, pulse frequency and circulating testosterone levels in hypotestosteronaemic men with type 2 diabetes
  • change in BMI was associated with the change in testosterone (Corona et al. 2013a,b).
  • weight loss can lead to genuine reactivation of the gonadal axis by reversal of obesity-associated hypothalamic suppression
  • There is pre-clinical and observational evidence that chronic hyperglycaemia can inhibit the HPT axis
  • in men who improved their glycaemic control over time, testosterone levels increased. By contrast, in those men in whom glycaemic control worsened, testosterone decreased
  • testosterone levels should be measured after successful weight loss to identify men with an insufficient rise in their testosterone levels. Such men may have HPT axis pathology unrelated to their obesity, which will require appropriate evaluation and management.
  • Nathan Goodyear on 04 Feb 14
     
    Article discusses the expanding evidence of low T and Metabolic syndrome.
Nathan Goodyear

Responses of Gut Microbiota and Glucose and Lipid Metabolism to Prebiotics in Genetic O... - 0 views

www.ncbi.nlm.nih.gov/...PMC3198091

prebiotics probiotic Bifidobacterium leptin resistance leptin glucose lipids inflammation LPS

shared by Nathan Goodyear on 05 Jun 16 - No Cached
  • Nathan Goodyear on 05 Jun 16
     
    prebiotics found to increase leptin sensitivity, improved glucose metabolism, lipid metabolism, reduced inflammation and improved leaky gut.  The probiotics increased the bifidobacterium species versus a decrease in the Firmicutes phyla.
Nathan Goodyear

Type 1 diabetes associated with acquired generaliz... [J Clin Endocrinol Metab. 2008] -... - 0 views

www.ncbi.nlm.nih.gov/...17940115

leptin insulin resistance hypertriglyceridemia diabetes

shared by Nathan Goodyear on 10 Mar 11 - No Cached
  • Acquired generalized lipodystrophy (AGL) is marked by severe insulin resistance and hypertriglyceridemia. Rarely, AGL and type 1 diabetes (T1D) coexist.
  • Long-term recombinant leptin therapy is effective in treating the insulin resistance of patients with the unusual combination of T1D and AGL.
  • Nathan Goodyear on 10 Mar 11
     
    leptin useful in severe insulin resistance, hypertriglyceridemia and type 1 Diabetes
Nathan Goodyear

Obesity - Relation of Leptin to Insulin Resistance Syndrome in Children - 0 views

www.nature.com/...oby2003153a.html

insulin resistance leptin childhood obesity IR children

shared by Nathan Goodyear on 15 Nov 11 - No Cached
  • Nathan Goodyear on 15 Nov 11
     
    leptin and insulin resistance and the web they play in childhood obesity
Nathan Goodyear

Leptin resistance is associated with extreme obesity and aggregates in families - 0 views

www.nature.com/...0801736a.html

leptin resistance obesity

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  • Nathan Goodyear on 09 Mar 11
     
    leptin resistance and obesity
Nathan Goodyear

Obesity - Leptin Resistance and Obesity - 0 views

www.nature.com/...oby2006319a.html

leptin resistance obesity

shared by Nathan Goodyear on 09 Mar 11 - No Cached
  • Nathan Goodyear on 09 Mar 11
     
    another great review on Leptin Resistance and obesity
Nathan Goodyear

Circumventing leptin resistance for weight control - 0 views

www.ncbi.nlm.nih.gov/...PMC33319

leptin resistance weight

shared by Nathan Goodyear on 09 Mar 11 - No Cached
  • Nathan Goodyear on 09 Mar 11
     
    how to correct leptin-resistance to improve weight loss; heavy read
Nathan Goodyear

Inflammation and insulin resistance 10.1016/j.febslet.2007.11.057 : FEBS Letters | Scie... - 0 views

www.sciencedirect.com/...S0014579307012082

inflammation insulin resistance IR PPAR TNF-alpha IL-6 IL-10 IL-1Beta JNK GLT-4 Resistin adiponectin Gherlin NF-kapppB iNOS lkkb obesity TLR-4

shared by Nathan Goodyear on 10 Jan 12 - No Cached
  • A subsequent study by Yuan et al. showed that Tnf treatment of 3T3L1 adipocytes induces insulin resistance and that this could be prevented by pretreatment of cells with aspirin
  • Activation of the Tnf receptor results in stimulation of NFκB signaling via Ikkb
  • Insulin is a pleiotropic hormone
  • ...25 more annotations...
  • the percentage of macrophages in a given adipose tissue depot is positively correlated with adiposity and adipocyte size
  • Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes
  • Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NFκB activation by reducing IKK activity [38]
  • adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression
  • One theory holds that the expansion of adipose tissue leads to adipocyte hypertrophy and hyperplasia and that large adipocytes outstrip the local oxygen supply leading to cell autonomous hypoxia with activation of cellular stress pathways
  • The use of the anti-inflammatory compounds, salicylate and its derivative aspirin, for treating symptoms of T2DM dates back over 100 years
  • elevated levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states
  • overnutrition and obesity are often accompanied by elevations in tissue and circulating FFA concentrations, and saturated FFAs can directly activate pro-inflammatory responses
  • Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity
  • In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter
  • macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the “classically activated” pro-inflammatory macrophage, to the M2 state or the “alternatively activated” non-inflammatory cell
  • saturated fatty acids are the most potent inducers of this inflammatory response
  • Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes iNOS (reviewed in [33]
  • Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes.
  • In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production
  • elevated JNK activity in liver, adipose tissue and skeletal muscle of obese insulin resistant mice, and knockout of Jnk1 (Jnk1−/−) leads to amelioration of insulin resistance in high fat diet
  • Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance
  • C-reactive protein (CRP)
  • these studies highlight the possibility that increased iNOS activity plays a direct role in the pathogenesis of insulin resistance
  • the important role of Ikkb in the development of obesity and inflammation-induced insulin resistance.
  • It is probable that local concentrations of inflammatory mediators, such as FFAs, Tnf or other cytokines/adipokines contribute to this polarity switch
  • Tnf and other cytokines/chemokines are symptomatic of inflammation, and while they propagate and/or maintain the inflammatory state, they are not the initial cause(s) of inflammation
  • Tlr4, in particular, is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria
  • Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system.
  • Tlr4 stimulation results in the activation of both Ikkb/NFκB and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1, etc. (reviewed in [57
  • Nathan Goodyear on 10 Jan 12
     
    Great review of all the known components in the inflammation, insulin resistance link
Nathan Goodyear

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

www.sciencedirect.com/...S1550413111003123

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

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

http://journals.cambridge.org/download.php?file=%2FBJN%2FBJN106_03%2FS000711451100033Xa... - 0 views

journals.cambridge.org/download.php

sugar fructose leptin leptin resistance diet nutrition obesity

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  • Nathan Goodyear on 05 Jun 16
     
    elimination of sugar, fructose in rat model found to reverse leptin resistance.
Nathan Goodyear

Journal of Clinical Investigation -- Pathophysiological role of leptin in obesity-relat... - 0 views

www.jci.org/...1

leptin resistance obesity hypertension

shared by Nathan Goodyear on 04 Mar 11 - No Cached
  • Nathan Goodyear on 04 Mar 11
     
    leptin-resistance as cause of obesity and contribution to hypertension
Nathan Goodyear

Cell Metabolism - Protein Tyrosine Phosphatase Epsilon Affects Body Weight by Downregul... - 0 views

www.cell.com/...S1550-4131(11)00139-2

leptin resistance obesity tyrosine phospatase epsilon

shared by Nathan Goodyear on 10 May 11 - No Cached
  • Nathan Goodyear on 10 May 11
     
    new insight on biochemistry of leptin resistance and obesity
Nathan Goodyear

Randomized, double blind placebo-controlled trial: effects of myo-inositol on ovarian f... - 0 views

www.mendeley.com/...n-metabolic-factors-women-pcos

myo-inositol weight loss leptin insulin overweight

shared by Nathan Goodyear on 01 Jun 11 - No Cached
  • significant weight loss (and leptin reduction) (P < 0.01) was recorded in the myo-inositol group, whereas the placebo group actually increased weight
  • hese data support a beneficial effect of myo-inositol in women with oligomenorrhea and polycystic ovaries in improving ovarian function.
  • Nathan Goodyear on 01 Jun 11
     
    myo-inositol improves weight loss and leptin resistance through insulin secondary messenger
Nathan Goodyear

Berberine Improves Insulin Sensitivity by Inhibiting Fat Store and Adjusting Adipokines... - 0 views

www.hindawi.com/...363845

berberine BMI obesity metabolic syndrome leptin leptin resistance insulin resistance adiponectin natural alternative

shared by Nathan Goodyear on 25 Mar 15 - No Cached
  • Nathan Goodyear on 25 Mar 15
     
    Berberine reduced BMI, improved insulin sensitivity, improved leptin sensitivity, and improved leptin:adiponectin ratio levels in people with metabolic syndrome after 3 months.
Nathan Goodyear

New mechanisms and the anti-inflammatory role of curcumin in obesity and obesity-relate... - 0 views

www.ncbi.nlm.nih.gov/...21442412

curcumin polyphenols obesity diabetes lipids inflammation leptin resistance adiponectin

shared by Nathan Goodyear on 05 Jun 16 - No Cached
  • Nathan Goodyear on 05 Jun 16
     
    Review article of Curcumin, a polyphenol, reduces insulin resistance, leptin resistance,  elevated glucose levels, elevated lipids, and inflammation in obesity and metabolic dysfunction.  Adiponectin levels were increased.
Nathan Goodyear

Thieme eJournals - Abstract - 0 views

www.thieme-connect.com/...s-2006-948308

vitamin D deficiency obesity insulin resistance leptin PCOS

shared by Nathan Goodyear on 10 Sep 11 - No Cached
  • Nathan Goodyear on 10 Sep 11
     
    vitamin D associated with obesity, insulin resistance, and leptin resistance in women with PCOS
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