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Nathan Goodyear

High normal plasma triglycerides are associated with preserved cognitive function in Ch... - 1 views

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    Higher triglyceride levels associated with better cognitive function versus those with lower triglyceride levels in an elderly chinese population.
Nathan Goodyear

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

  • 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
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  • 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
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    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

Triglycerides Induce Leptin Resistance at the Blood-Brain Barrier - 0 views

  • Obesity is associated with leptin resistance
  • Resistance arises from impaired leptin transport across the blood-brain barrier (BBB)
  • Decreasing triglycerides may potentiate the anorectic effect of leptin by enhancing leptin transport across the BBB.
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  • Starvation, like obesity, is accompanied by a decreased BBB transport rate of exogenous leptin
  • hypertriglyceridemia could explain impaired transport of leptin across the BBB in both starvation and obesity
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    elevated triglycerides and leptin resistance
Nathan Goodyear

Medium Chain Triglycerides (MCTs) | Nutrition Review - 0 views

  • lower caloric content than LCTs
  • MCTs are not stored in fat deposits in the body as much as LCTs
  • MCTs have been shown to enhance thermogenesis
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    great review of medium chain triglycerides.
Nathan Goodyear

Effects of exogenous ketone supplementation on blood ketone, glucose, triglyceride, and... - 0 views

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    animal study finds increased BHB after ketone salt supplementation.  A resultant decrease in glucose was found.  The use of ketone salts was with concomitant MCT.  The effect was in 30-60 minutes and sustained, significantly for 8 hours.  Weight loss was also seen.  No change in cholesterol and triglycerides was seen.
Nathan Goodyear

Determinants of intramyocellular triglyceride turnover: implications for insulin sensit... - 0 views

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    insulin sensitivity, triglyceride turnover and energy
Nathan Goodyear

Exercise training-induced triglyceride lowering negatively correlates with DHEA levels ... - 0 views

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    aerobic exercise over 8 weeks increased DHEA modestly.  An inverse relationship between DHEA and Triglycerides was seen.
Nathan Goodyear

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

  • Weight gain has been associated with a higher gut permeability
  • a high-fat diet promotes LPS absorption
  • higher concentrations of fatty acids impair intestinal barrier integrity
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  • The starting point for innate immunity activation is the recognition of conserved structures of bacteria, viruses, and fungal components through pattern-recognition receptors
  • TLRs are PRRs that recognize microbe-associated molecular patterns
  • TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain homologous to the IL1 receptor intracellular domain
  • The major proinflammatory mediators produced by the TLR4 activation in response to endotoxin (LPS) are TNFα, IL1β and IL6, which are also elevated in obese and insulin-resistant patients
  • Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
  • Probiotics, prebiotics, and antibiotic treatment can reduce LPS absorption
  • LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease.
  • In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression.
  • In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
  • the gut microbiota has been recently proposed to be an environmental factor involved in the control of body weight and energy homeostasis by modulating plasma LPS levels
  • dietary fats alone might not be sufficient to cause overweight and obesity, suggesting that a bacterially related factor might be responsible for high-fat diet-induced obesity.
  • This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in Bifidobacterium and Eubacterium spp.
  • n humans, it was also shown that meals with high-fat and high-carbohydrate content (fast-food style western diet) were able to decrease bifidobacteria levels and increase intestinal permeability and LPS concentrations
  • it was demonstrated that, more than the fat amount, its composition was a critical modulator of ME (Laugerette et al. 2012). Very recently, Mani et al. (2013) demonstrated that LPS concentration was increased by a meal rich in saturated fatty acids (SFA), while decreased after a meal rich in n-3 polyunsaturated fatty acids (n-3 PUFA).
  • this effect seems to be due to the fact that some SFA (e.g., lauric and mystiric acids) are part of the lipid-A component of LPS and also to n-3 PUFA's role on reducing LPS potency when substituting SFA in lipid-A
  • these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of LPS-mediated nutritional changes.
  • This suggests a link between gut microbiota, western diet, and obesity and indicates that gut microbiota manipulation can beneficially affect the host's weight and adiposity.
  • endotoxemia was independently associated with energy intake but not fat intake in a multivariate analysis
  • in vitro that endotoxemia activates pro-inflammatory cytokine/chemokine production via NFκB and MAPK signaling in preadipocytes and decreased peroxisome proliferator-activated receptor γ activity and insulin responsiveness in adipocytes.
  • T2DM patients have mean values of LPS that are 76% higher than healthy controls
  • LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both peripheral and hepatic
  • LPSs also seem to induce ROS-mediated apoptosis in pancreatic cells
  • Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression of alcoholic and nonalcoholic fatty liver disease
  • The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted in bile
  • All the subclasses of plasma lipoproteins can bind and neutralize the toxic effects of LPS, both in vitro (Eichbaum et al. 1991) and in vivo (Harris et al. 1990), and this phenomenon seems to be dependent on the number of phospholipids in the lipoprotein surface (Levels et al. 2001). LDL seems to be involved in LPS clearance, but this antiatherogenic effect is outweighed by its proatherogenic features
  • LPS produces hypertriglyceridemia by several mechanisms, depending on LPS concentration. In animal models, low-dose LPS increases hepatic lipoprotein (such as VLDL) synthesis, whereas high-dose LPS decreases lipoprotein catabolism
  • When a dose of LPS similar to that observed in ME was infused in humans, a 2.5-fold increase in endothelial lipase was observed, with consequent reduction in total and HDL. This mechanism may explain low HDL levels in ‘ME’ and other inflammatory conditions such as obesity and metabolic syndrome
  • It is known that the high-fat diet and the ‘ME’ increase intrahepatic triglyceride accumulation, thus synergistically contributing to the development and progression of alcoholic and NAFLD, from the initial stages characterized by intrahepatic triglyceride accumulation up to chronic inflammation (nonalcoholic steatohepatitis), fibrosis, and cirrhosis
  • On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines like TNFα
  • high-fat diet mice presented with ME, which positively and significantly correlated with plasminogen activator inhibitor (PAI-1), IL1, TNFα, STAMP2, NADPHox, MCP-1, and F4/80 (a specific marker of mature macrophages) mRNAs
  • prebiotic administration reduces intestinal permeability to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
  • Cani et al. also found that high-fat diet mice presented with not only ME but also higher levels of inflammatory markers, oxidative stress, and macrophage infiltration markers
  • This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat diet situation
  • high-fat feeding is associated with adipose tissue macrophage infiltration (F4/80-positive cells) and increased levels of chemokine MCP-1, suggesting a strong link between ME, proinflammatory status, oxidative stress, and, lately, increased CV risk
  • LPS has been shown to promote atherosclerosis
  • markers of systemic inflammation such as circulating bacterial endotoxin were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
  • As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory state.
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    Very nice updated review on Metabolic endotoxemia
Nathan Goodyear

The effect of plant sterols on serum triglyceride concentrations is dependent on baseli... - 0 views

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    plant sterols lower triglycerides.
Nathan Goodyear

Triglyceride-Lowering Response To Plant Sterol and Stanol Consumption - 0 views

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    plant sterols lower triglycerides as well as LDL and total cholesterol.
Nathan Goodyear

Journal of Endocrinological Investigation - 0 views

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    vitamin D therapy shown to reduce total cholesterol and triglycerides in those with low vitamin D levels.
Nathan Goodyear

Dehydroepiandrosterone (DHEA) replacement decreases insulin resistance and lowers infla... - 0 views

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    DHEA declines with age.  DHEA therapy, 50 mg daily, was found to reduce TNF-alpha and IL-6.  DHEA also lowered triglycerides.
Nathan Goodyear

High-fructose diet leads to visceral adiposity and hypothalamic leptin resistance in ma... - 0 views

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    high fructose diet for just 9 weeks, > 60% liquid fructose, in rat model found to increase visceral adiposity, triglycerides, and lead to leptin resistance.
Nathan Goodyear

Two-year changes in lipids and lipoproteins associa... [Obes Res. 1999] - PubMed - NCBI - 0 views

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    Weight loss improves lipid profile.  Total cholesterol, LDL, and triglycerides were reduced with weight loss of 5-10%.  However, weight loss exceeding 10% resulted in greater reduction and longer maintenance of the improved lipid panel results.
Nathan Goodyear

Dietary Strategies for Improving Post-Prandial Glucose, Lipids, Inflammation, and Cardi... - 0 views

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    Diet can be a direct cause of inflammation.  A anti-inflammatory diet is a must in those with chronic, inflammatory diseases.    In this study, triglycerides, oxidative stress, and inflammation was found immediately after a single meal of saturated fat.
Nathan Goodyear

Figure 2 : Adipocyte dysfunctions linking obesity to insulin resistance and t... - 0 views

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    chronic, not acute, inflammation disrupts normal triglyceride metabolism and results in increased FFA
Nathan Goodyear

Niacin in Patients with Low HDL Cholesterol Levels Receiving Intensive Statin Therapy -... - 0 views

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    clients on statin therapy shown to have significant further decrease in triglycerides and increase in HDL in AIM-HIGH study.
Nathan Goodyear

JAMA Network | JAMA: The Journal of the American Medical Association | Effects of Prote... - 0 views

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    In this study, a high carbohydrate diet was replaced with a diet higher in monosaturated fats.  The result was: a lower carb diet with resultant increase in monosaturated fats resulted in a reduction in triglycerides, reduction in systolic B/P, increase in HDL, and resultant decrease in CVD risk
Nathan Goodyear

Endogenous sex hormones and cardiovascular disease in men. A prospective population-bas... - 0 views

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    This study found that Testosterone levels were inversely associated with hypertension, fasting glucose, triglycerides, and BMI.
Nathan Goodyear

Association between plasma total tes... [J Clin Endocrinol Metab. 1997] - PubMed - NCBI - 0 views

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    low Total Testosterone associated with increased BMI, systolic blood pressure, glucose, triglycerides, total cholesterol, LDL apolipoprotien B and A1. Low Testosterone is associated with increased cardiovascular disease.  Men at risk for cardiovascular disease must be evaluated for hormones.
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