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Nathan Goodyear

Metabolic syndrome, circulating RBP4, testosterone, and SHBG predict weight regain at 6... - 0 views

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    Interesting study finds that men with low serum Total Testosterone, elevated RBP4 and low SHBG at baseline predict weight regain.  Thus Testosterone should be used as a biomarker of failure in weight loss and if low, Testosterone therapy should be employed to improved metabolic function.  Other parameters, such as leptin, adiponectin, prolactin, progesterone...were not predictive.
Nathan Goodyear

PLOS ONE: Prediabetes Is Associated with an Increased Risk of Testosterone Deficiency, ... - 0 views

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    This study found that low T was clearly associated with "pre diabetes" independent of weight and MetS.  All men that are overweight, obese, with metabolic syndrome, "pre diabetic" need evaluation of hormones, not just Testosterone.
Nathan Goodyear

Toll-like receptor signaling links dietary fatty acids to the metabolic syndrome - 0 views

  • Activation of the innate immune system controls macronutrient metabolism
  • the innate immune response is the first line of defense against invading pathogens, wherein highly conserved pathogen-associated molecular patterns (PAMPs) are recognized by cognate pattern recognition receptors (PRRs
  • many studies have supported the idea that cytokine signaling directly promotes insulin resistance
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  • innate immune system may be causally linked to obesity
  • adipose tissue contains a substantial population of macrophages, and macrophage-driven adipose inflammation contributes significantly to the pathogenesis of obesity
  • Collectively, activation of the innate immune system is strongly associated with ASCVD, insulin resistance, and obesity, and recent evidence suggests that much of this association can be traced to a unique family of PRRs known as TLRs
  • TLRs are a family of type I transmembrane receptors, currently thought to comprise at least 13 members in mammals, that specifically recognize a variety of microbial PAMPs and trigger host cellular responses
  • Free SFAs have indeed been demonstrated to elicit TLR4-dependent and TLR2-dependent responses in several cell types.
  • Endogenous SFAs released from adipocytes activate cocultured macrophages via TLR4 [], indicating the potential for cellular crosstalk in adipose tissue. Collectively, there is a growing body of evidence that SFAs promote, whereas long chain PUFA antagonize, TLR4-dependent and TLR2-dependent signaling in multiple cell models
  • In an elegant study, Shi et al. [] demonstrated that SFAs activate TLR4-dependent signaling in both macrophages and adipocytes, and mice lacking TLR4 are protected against insulin resistance driven by intravenous lipid infusion
  • In addition to effects in macrophages and adipocytes, SFAs can activate TLR4 in the hypothalamus, which triggers a central inflammatory response that results in resistance to anorexigenic signals
  • endogenous SFAs can indeed promote innate immunity and inflammatory disease
  • This finding strongly supports the work of Hwang and coworkers [] demonstrating that ω-3 PUFAs can effectively counteract SFA-induced TLR4 activation in cultured macrophages and dendritic cells.
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    high dietary fatty acids linked to metabolic syndrome through TLR.
Nathan Goodyear

Clinical Importance of Obesity Versus the Metabolic Syndrome in Cardiovascular Risk in ... - 0 views

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    weight loss improves metabolic syndrome, which results in reduced cardiovascular disease
Nathan Goodyear

Adrenocortical dysregulation as a major player in insulin resistance and onset of obesity - 0 views

  • acute GC secretion during stress mobilizes peripheral amino acids from muscle as well as fatty acids and glycerol from peripheral fat stores to provide substrates for glucose synthesis by the liver
  • chronically elevated GC levels alter body fat distribution and increase visceral adiposity as well as metabolic abnormalities in a fashion reminiscent of metabolic syndrome
  • This local production may play an important role in the onset of obesity and insulin resistance.
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  • In adipocytes, cortisol inhibits lipid mobilization in the presence of insulin, thus leading to triglyceride accumulation and retention.
  • Since the density of GC receptors is higher in intra-abdominal (visceral) fat than in other fat depots, the activity of cortisol leading to accumulation of fat is accentuated in visceral adipose tissue (24, 158), providing a mechanism by which excessive endogenous or exogenous GC lead to abdominal obesity and IR
  • obese patients generally have normal or subnormal plasma cortisol concentrations
  • This may be explained by an increased intratissular/cellular concentration of cortisol in adipose tissues
  • Intracellular GC may be produced from recycling of GC metabolites such as cortisone in adipose tissues
  • Local GC recycling metabolism is mediated by 11β-hydroxysteroid dehydrogenase enzymes (11β-HSD1 and 11β-HSD2
  • Cortisol also increases 11β-HSD1 expression in human adipocytes
  • In humans, elevated 11β-HSD1 expression in visceral adipose tissue is also associated with obesity
  • even if obese patients generally have normal or subnormal plasma cortisol concentrations (131, 158), triglyceride accumulation in visceral adipose tissue may be due, at least in part, to the local production of GC in insulin- and GC-responsive organs such as adipose tissue, liver, and skeletal muscle
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    another nice article on the dysregulation of cortisol and its role in insulin resistance, metabolic syndrome, and obesity.
Nathan Goodyear

Increased Toll-Like Receptor Activity in Patients With Metabolic Syndrome - 0 views

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    TLR2 and TLR4 are increased in patients with metabolic syndrome.  No surprise that IL-1Beta, IL-6, IL-8, TNF-alpha were increased as well.
Nathan Goodyear

International Journal of Impotence Research - Abstract of article: Epidemiology: testos... - 0 views

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    low Testosterone shown to be associated with insulin resistance, poor glucose control, elevated HgbA1c, and obesity
Nathan Goodyear

Interplay between obesity and associated metabolic disorders: new insights into the gut... - 0 views

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    This article discusses the link between the gut flora, inflammation, and metabolic endotoxmia resulting in obesity and other inflammatory diseases of aging.
Nathan Goodyear

JCI - Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the me... - 0 views

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    great read on the relationship of adiponectin and insulin resistance, metabolic syndrome, diabetes,  and obesity.
Nathan Goodyear

BMC Public Health | Abstract | High prevalence of vitamin D insufficiency and its assoc... - 0 views

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    Malaysians with metabolic syndrome and obesity found to have high prevalence of vitamin D insufficiency.  Role for vitamin D therapy for those with metabolic syndrome and obesity.
Nathan Goodyear

Association between the Metabolic Syndrome and Serum Cortisol in Overweight Latino Youth - 0 views

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    As the number of components of metabolic syndrome increase: so does the am cortisol in children
Nathan Goodyear

Endocrine and metabolic effects of consuming bever... [Am J Clin Nutr. 2008] - PubMed r... - 0 views

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    fructose, HCFS, and sucrose increase triglyceride formation = fat
Nathan Goodyear

Epidemiology of non-alcoholic fatty liver disease. [Dig Dis. 2010] - PubMed result - 0 views

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    non-alcoholic fatty liver disease the result of Metabolic syndrome.  New epidemic associated with obesity.

    Scary statistics about the children of America.
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