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Nathan Goodyear

Branched-Chain Amino Acid Supplementation in Patients with Liver Diseases - 0 views

jn.nutrition.org/...1596S.long

BCAA branched chain amino acids amino acids liver cirrhosis

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • the optimum amount of BCAA supplements for liver disease has not been determined,
  • BCAAs not only provide substrates for protein synthesis but also accelerate the biochemical machinery, which facilitates liver regeneration, compensating for progressive liver-cell death
  • rapamycin signaling in the liver, a well-demonstrated effect of BCAAs, promotes albumin synthesis in the liver
  • ...1 more annotation...
  • the amount of BCAAs supplied in the various studies is extremely variable
  • Nathan Goodyear on 05 Oct 15
     
    BCAA effective in patients with liver cirrhosis, liver cancer, and liver transplant.  BCAA improve the liver regenerative capacity.
Nathan Goodyear

Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2... - 0 views

www.nature.com/...s41698-017-0044-8

cancer cancer stem cells liver cancer vitamin C IV vitamin C oncology

shared by Nathan Goodyear on 30 Jan 18 - No Cached
  • Chen et al. have revealed that ascorbate at pharmacologic concentrations (0.3–20 mM) achieved only by intravenously (i.v.) administration selectively kills a variety of cancer cell lines in vitro, but has little cytotoxic effect on normal cells.
  • Ascorbic acid (the reduced form of vitamin C) is specifically transported into cells by sodium-dependent vitamin C transporters (SVCTs)
  • SVCT-1 is predominantly expressed in epithelial tissues
  • ...41 more annotations...
  • whereas the expression of SVCT-2 is ubiquitous
  • differential sensitivity to VC may result from variations in VC flow into cells, which is dependent on SVCT-2 expression.
  • high-dose VC significantly impaired both the tumorspheres initiation (Fig. 4d, e) and the growth of established tumorspheres derived from HCC cells (Fig. 4f, g) in a time-dependent and dose-dependent manner.
  • Hepatocellular carcinoma (HCC)
  • The antioxidant, N-acetyl-L-cysteine (NAC), preventing VC-induced ROS production (a ROS scavenger), completely restored the viability and colony formation among VC-treated cells
  • DNA double-strand damage was found following VC treatment
  • DNA damage was prevented by NAC
  • Interestingly, the combination of VC and cisplatin was even more effective in reducing tumor growth and weight
  • Consistent with the in vitro results, stemness-related genes expressions in tumor xenograft were remarkably reduced after VC or VC+cisplatin treatment, whereas conventional cisplatin therapy alone led to the increase of CSCs
  • VC is one of the numerous common hepatoprotectants.
  • Interestingly, at extracellular concentrations greater than 1 mM, VC induces strong cytotoxicity to cancer cells including liver cancer cells
  • we hypothesized that intravenous VC might reduce the risk of recurrence in HCC patients after curative liver resection.
  • Intriguingly, the 5-year disease-free survival (DFS) for patients who received intravenous VC was 24%, as opposed to 15% for no intravenous VC-treated patients
  • Median DFS time for VC users was 25.2 vs. 18 months for VC non-users
  • intravenous VC use is linked to improved DFS in HCC patients.
  • In this study, based on the elevated expression of SVCT-2, which is responsible for VC uptake, in liver CSCs, we revealed that clinically achievable concentrations of VC preferentially eradicated liver CSCs in vitro and in vivo
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      the authors here made similar mistakes to the Mayo authors i.e. under doses here in this study.  They dosed at only 2 grams IVC.  A woefully low dose of IVC.
  • Additionally, we found that intravenous VC reduced the risk of post-surgical HCC progression in a retrospective cohort study.
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      positive results despite a low dose used.
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      Their comfort zone was 1mM.  They should have targeted 20-40 mM.
  • Three hundred thirty-nine participants (55.3%) received 2 g intravenous VC for 4 or more days after initial hepatectomy
  • As the key protein responsible for VC uptake in the liver, SVCT-2 played crucial roles in regulating the sensitivity to ascorbate-induced cytotoxicity
  • we also observed that SVCT-2 was highly expressed in human HCC samples and preferentially elevated in liver CSCs
  • SVCT-2 might serve as a potential CSC marker and therapeutic target in HCC
  • CSCs play critical roles in regulating tumor initiation, relapse, and chemoresistance
  • we revealed that VC treatment dramatically reduced the self-renewal ability, expression levels of CSC-associated genes, and percentages of CSCs in HCC, indicating that CSCs were more susceptible to VC-induced cell death
  • as a drug for eradicating CSCs, VC may represent a promising strategy for treatment of HCC, alone or particularly in combination with chemotherapeutic drugs
  • In HCC, we found that VC-generated ROS caused genotoxic stress (DNA damage) and metabolic stress (ATP depletion), which further activated the cyclin-dependent kinase inhibitor p21, leading to G2/M phase cell cycle arrest and caspase-dependent apoptosis in HCC cells
  • we demonstrated a synergistic effect of VC and chemotherapeutic drug cisplatin on killing HCC both in vitro and in vivo
  • Intravenous VC has also been reported to reduce chemotherapy-associated toxicity of carboplatin and paclitaxel in patients,38 but the specific mechanism needs further investigation
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      so, exclude the benefit to patients until the exact mechanism of action, which will never be fully elicited?!?!?
  • Our retrospective cohort study also showed that intravenous VC use (2 g) was related to the improved DFS in HCC patients after initial hepatectomy
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      Terribly inadequate dose.  Target is 20-40 mM which other studies have found occur with 50-75 grams of IVC.
  • several clinical trials of high-dose intravenous VC have been conducted in patients with advanced cancer and have revealed improved quality of life and prolonged OS
  • high-dose VC was not toxic to immune cells and major immune cell subpopulations in vivo
  • high recurrence rate and heterogeneity
  • tumor progression, metastasis, and chemotherapy-resistance
  • SVCT-2 was highly expressed in HCC samples in comparison to peri-tumor tissues
  • high expression (grade 2+/3+) of SVCT-2 was in agreement with poorer overall survival (OS) of HCC patients (Fig. 1c) and more aggressive tumor behavior
  • SVCT-2 is enriched in liver CSCs
  • these data suggest that SVCT-2 is preferentially expressed in liver CSCs and is required for the maintenance of liver CSCs.
  • pharmacologic concentrations of plasma VC higher than 0.3 mM are achievable only from i.v. administration
  • The viabilities of HCC cells were dramatically decreased after exposure to VC in dose-dependent manner
  • VC and cisplatin combination further caused cell apoptosis in tumor xenograft
  • These results verify that VC inhibits tumor growth in HCC PDX models and SVCT-2 expression level is associated with VC response
  • qPCR and IHC analysis demonstrated that expression levels of CSC-associated genes and percentages of CSCs in PDXs dramatically declined after VC treatment, confirming the inhibitory role of VC in liver CSCs
  • Nathan Goodyear on 30 Jan 18
     
    IV vitamin C in vitro and in vivo found to "preferentially" eradicate cancer stem cells.  In addition, IV vitamin C was found to be adjunctive to chemotherapy, found to be hepatoprotectant.  This study also looked at SVCT-2, which is the transport protein important in liver C uptake.
Nathan Goodyear

Association Between Endogenous Sex Hormones and Liver Fat in a Mult... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25592661

Testosterone Estradiol SHBG hormone hormones men women non-alcoholic fatty liver fatty liver CVD cardiovascular disease cardiovascular disease

shared by Nathan Goodyear on 02 Feb 15 - No Cached
  • Nathan Goodyear on 02 Feb 15
     
    Time that physicians start following the science.  Study using data from the Multi-ethnic Study of Atherosclerosis was used to assess hormones and fatty liver in men and women.  Increasing bioavailable Testosterone levels in women was found to be associated with increasing fatty liver in post-menopausal women.  The opposite was found to be true in men.  Higher Estradiol levels were found to be associated with increased fatty liver in both sexes.  However, the statistical significance was higher with men.  Higher SHBG was associated with lower fatty liver incidence in men.  
Nathan Goodyear

Branched Chain Amino Acid Supplementation for Patients with Cirrhosis | Clinical Correl... - 0 views

www.clinicalcorrelations.org/?p=3544

BCCA branched chain amino acids liver cirrhosis hepatitis amino acids

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • low level of BCAAs in patients with cirrhosis is hypothesized to be one of multiple factors responsible for development of hepatic encephalopathy
  • supplementation of BCAAs is thought to facilitate ammonia detoxification by supporting synthesis of glutamine, one of the non-branched chain amino acids, in skeletal muscle and in the brain as well as diminishing the influx of AAAs across the blood-brain barrier
  • oral BCAA supplementation is more useful in chronic encephalopathic patients than is parenteral BCAA supplementation in patients with acute encephalopathy
  • ...35 more annotations...
  • malnutrition progressing to cachexia is another common manifestation of cirrhosis
  • Malnutrition can be mitigated with BCAA supplementation
  • Studies show that administration of amino acid formulas enriched with BCAAs can reduce protein loss, support protein synthesis, and improve nutritional status of patients with chronic liver disease
  • Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis
  • BCAAs metabolites inhibit proteolysis
  • Patients with cirrhosis have both insulin deficiency and insulin resistance
  • BCAAs (particularly leucine) help to reverse the catabolic, hyperglucagonemic state of cirrhosis both by stimulating insulin release from the pancreatic β cells and by decreasing insulin resistance allowing for better glucose utilization
  • Coadministration of BCAAs and glucose has been found to be particularly useful
  • BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis
  • Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity
  • another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity
  • BCAA supplementation may reduce the risk of infection in patients with advanced cirrhosis not only through improvement in protein-energy malnutrition but also by directly improving the function of the immune cells themselves
  • BCAA administration has also been shown to have a positive effect on liver regeneration
  • A proposed mechanism for improved liver regeneration is the stimulatory effect of BCAAs (particularly leucine) on the secretion of hepatocyte growth factor by hepatic stellate cells
  • BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue
  • Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels
  • long-term oral BCAA supplementation was useful in staving off malnutrition and improving survival by preventing end-stage fatal complications of cirrhosis such as hepatic failure and gastrointestinal bleeding
  • The incidence of death by any cause, development of liver cancer, rupture of esophageal varices, or progression to hepatic failure was decreased in the group that received BCAA supplementation
  • Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests
  • patients taking BCAA supplementation report improved quality of life
  • BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis
  • BCAAs make up 20-25% of the protein content of most foods
  • Highest levels are found in casein whey protein of dairy products and vegetables, such as corn and mushrooms. Other sources include egg albumin, beans, peanuts and brown rice bran
  • In addition to BCAAs from diet, oral supplements of BCAAs can be used
  • Oral supplementation tends to provide a better hepatic supply of BCAAs for patients able to tolerate PO nutrition as compared with IV supplementation, especially when treating symptoms of hepatic encephalopathy
  • Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms
  • Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state
  • the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting
  • A late night nutritional snack reduces symptoms of weakness and fatigability, lowers postprandial hyperglycemia, increases skeletal muscle mass,[25] improves nitrogen balance, and increases serum albumin levels.[26] Nocturnal BCAAs even improve serum albumin in cirrhotic patients who show no improvement with daytime BCAAs
  • Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis
  • hyperglucagonemia results in a catabolic state eventually producing anorexia and cachexia
  • BCAAs are further depleted from the circulation due to increased uptake by skeletal muscles that use the BCAAs in the synthesis of glutamine, which is produced in order to clear the ammonia that is not cleared by the failing liver
  • patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation
  • Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life
  • the serum BCAA concentration is strongly correlated with the serum albumin level
  • Nathan Goodyear on 05 Oct 15
     
    great review of cirrhosis and BCCA supplementation.
Nathan Goodyear

Fructose Consumption as a Risk Factor for Non-alcoholic Fatty Liver Disease - 0 views

www.ncbi.nlm.nih.gov/...PMC2423467

fructose fructokinase triglyceride NAFLD non-alcoholic fatty liver fatty liver liver

shared by Nathan Goodyear on 01 Oct 13 - No Cached
  • Nathan Goodyear on 01 Oct 13
     
    Fructose upregulates fructokinase activity and this increase liver triglyceride production increasing non-alcoholic fatty liver disease also known as NAFLD.
Nathan Goodyear

Prevalence of Fatty Liver in Children and Adolescents - 0 views

pediatrics.aappublications.org/...1388

fatty liver children pediatrics adolescents

shared by Nathan Goodyear on 25 Aug 11 - No Cached
  • Fatty liver is the most common liver abnormality in children age 2 to 19 years
  • Nathan Goodyear on 25 Aug 11
     
    Fatty liver is most common liver abnormality in children 2 - 19.  Accounting for 13% of children in this study
Nathan Goodyear

Cancer stem cells in the development of liver cancer - 0 views

www.ncbi.nlm.nih.gov/...PMC3635728

cancer liver cancer CSC cancer stem cells liver

shared by Nathan Goodyear on 01 Feb 18 - No Cached
  • the finding of a stem cell–like gene expression signature is of great interest because it reflects the malignant nature of a tumor with poor survival outcome
  • poor prognosis of HCC in patients with stemness-associated gene expression traits is assumed to reflect the abundance of liver CSCs with highly tumorigenic and/or metastatic features
  • CSCs have a highly invasive and metastatic capacity
  • ...1 more annotation...
  • The discovery and exploration of liver CSCs has expanded our knowledge of the mechanisms by which liver cancers obtain tumorigenic, metastatic, and chemotherapy- and radiation-resistant capacities
  • Nathan Goodyear on 01 Feb 18
     
    Good review and discussion of liver cancer Cancer Stem cells.
Nathan Goodyear

[Glutathione in the treatment of ch... [Recenti Prog Med. 1995 Jul-Aug] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...7569285

IV glutathione detoxification fatty liver disease NAFLD

shared by Nathan Goodyear on 10 Nov 11 - No Cached
  • Nathan Goodyear on 10 Nov 11
     
    high dose IV glutathione shown to reduce liver enzymes and thus liver cell damage in those with chronic fatty liver disease
Nathan Goodyear

Uric acid induces hepatic steatosis by generatio... [J Biol Chem. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...23035112

uric acid mitochondria non-alcoholic fatty liver fructose triglyceride oxidative stress fatty liver liver ATP

shared by Nathan Goodyear on 01 Oct 13 - No Cached
  • Nathan Goodyear on 01 Oct 13
     
    Elevated uric acid levels up regulate fructose metabolism to triglycerides and fatty liver.  This study finds that liver mitochondrial oxidative stress is also evident.  This mitochondrial dysfunction also leads to compromised ATP production and fat accumulation specifically through inhibition of aconitase..
Nathan Goodyear

Branched-chain amino acids in liver diseases - 0 views

www.ncbi.nlm.nih.gov/...PMC3837260

BCAA branched chain amino acids liver cirrhosis disease

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Serum concentrations of BCAAs are decreased, while the concentrations of the aromatic amino acids (AAAs) phenylalanine and tyrosine are increased, in patients with advanced liver diseases, resulting in a low ratio of BCAAs to AAAs, a ratio called the Fischer ratio
  • BCAAs were reported to stimulate the production of hepatocyte growth factor
  • a simplified Fischer ratio, the BCAA to tyrosine ratio (BTR), has been reported useful for predicting serum albumin concentration one year later
  • ...10 more annotations...
  • BCAA supplementation was shown to delay the progression of CCl4-induced chronic liver injury in a rat model by reducing hepatic apoptosis
  • BCAAs promoted hepatocyte regeneration in a rat model of hepatectomy
  • BCAA supplementation for advanced cirrhotic patients improves nutritional status and quality of life
  • BCAAs activate mTOR and subsequently increase the production of eukaryotic initiation factor 4E-binding protein-1 and ribosomal protein S6 kinase, which upregulate the synthesis of albumin
  • BCAAs were shown to improve homeostasis model assessment scores for insulin resistance (HOMA-IR) and beta cell function (HOMA-%B) in patients with chronic liver disease, indicating that BCAAs can ameliorate insulin resistance
  • Several clinical trials have suggested that BCAA supplementation improves the prognosis of cirrhotic patients
  • A low Fischer ratio has been associated with hepatic encephalopathy
  • Treatment with BCAAs may therefore have a beneficial effect on patients with hepatic encephalopathy mainly by compensating decreased ratio of BCAAs to AAAs, but not by reducing serum ammonia levels
  • Two randomized studies also showed that BCAAs did not clearly prevent HE in patients with advanced cirrhosis, although BCAAs prevented the progression of hepatic failure
  • a systematic review with meta-analyses on the effect of oral BCAAs for the treatment of HE was published[66]. The review has revealed that supplementation of oral BCAAs in cirrhotic patients inhibits the manifestation of HE, especially in patients with overt HE rather than those with minimal HE, but showed no effect on the survival of those patients[66]. Thus, oral administration of BCAAs is the treatment of choice in cirrhotic patients with HE
  • Nathan Goodyear on 05 Oct 15
     
    good review of BCAA and liver disease: both mechanisms and therapy.
Nathan Goodyear

A case of amoxicillin-induced hepatocellular liver injury with bile-duct damage - 0 views

www.ncbi.nlm.nih.gov/...PMC3304646

amoxil amoxicillin liver antiobioitic liver enzymes

shared by Nathan Goodyear on 16 Apr 15 - No Cached
  • Nathan Goodyear on 16 Apr 15
     
    amoxil induced liver injury manifest with elevated liver enzymes.
Nathan Goodyear

Long term administration of a licorice extract in the treatment of - 0 views

www.greenmedinfo.com/...patitis-c-effective-preventi-0

licorice licorice root extract liver enzymes liver cirrhosis liver Hepatitis C HCV hepatitis

shared by Nathan Goodyear on 10 Sep 14 - No Cached
  • Nathan Goodyear on 10 Sep 14
     
    Licorice root extract shown to significantly reduce liver enzymes in those with chronic hepatitis C and to prevent progression to liver cirrhosis.  
Nathan Goodyear

Annals of Occupational and Environmental Medicine | Full text | The Relationship of Liv... - 0 views

www.aoemj.com/5

lead liver enzymes liver ALT AST environmental toxins

shared by Nathan Goodyear on 09 Mar 15 - No Cached
  • Nathan Goodyear on 09 Mar 15
     
    Lead and organic solvent exposure associated with increased liver function tests, indicating liver damage.
Nathan Goodyear

Unintended effects of statins from observational studies in the general population: sys... - 0 views

www.ncbi.nlm.nih.gov/...PMC3998050

statin therapy statins myopathy cholesterol side effects diabetes liver liver enzymes

shared by Nathan Goodyear on 19 Mar 15 - No Cached
  • A markedly increased risk of myopathy was observed
  • One cohort study (Women’s Health Initiative) of higher quality and larger sample size found stronger evidence of an increased risk of self-reported T2DM (OR=1.47; 95% CI 1.32 to 1.64) for the groups of women who reported statin use at baseline and three years later
  • Hippisley-Cox et al. found an increased risk of liver enzyme changes
  • ...5 more annotations...
  • weak evidence of an increased risk of type 2 diabetes mellitus (T2DM) was observed
  • Smeeth et al. found an increased risk of incident liver disease in the first year after the index date
  • The cumulative incidence of T2DM after three years of statin treatment was 6.25%, corresponding to an excess risk of 2.25%
  • We found no increased risk of peripheral neuropathy, depression, common eye diseases, renal disorders or arthritis associated with taking statins. Studies of higher quality did not show previously reported protective effects of statins on fractures, venous thrombo-embolism or pneumonia
  • There was evidence of an increase in myopathy, raised liver enzymes and diabetes.
  • Nathan Goodyear on 19 Mar 15
     
    Statin use associated with increased myopathy, liver dysfunction, and type II Diabetes.  The authors conclude that the absolute risk is very low, yet OR was 1.47 for type II Diabetes (translated 47% increased odds of developing Diabetes as a result of statins) and OR of 2.63 in risk of myopathy (translated 163% increased odds of developing myopathy as a result of statins).  Seems the authors "low risk" statement is just applies to those without symptoms/side effects.  Physicians need to do a better job of understanding risks and customizing therapies.
Nathan Goodyear

N-Acetylcysteine Improves Liver Function in Patients with Non-Alcoholic Fatty Liver Dis... - 0 views

www.ncbi.nlm.nih.gov/...PMC3270338

NAC N-acetylcysteine NAFLD non-alcoholic fatty liver fatty liver liver enzymes

shared by Nathan Goodyear on 17 Jul 18 - No Cached
  • Nathan Goodyear on 17 Jul 18
     
    Oral NAC useful for elevated liver enzymes in NAFLD
Nathan Goodyear

Hypercalcemia: A Complication of Advanced Chronic Liver Disease | JAMA Internal Medicin... - 0 views

jamanetwork.com/...607804

liver hypercalcemia liver disease

shared by Nathan Goodyear on 21 Aug 18 - No Cached
  • Nathan Goodyear on 21 Aug 18
     
    Hypercalcemia is a common finding in liver disease, especially cancer of the liver, whether primary or mets.  Also, consider hyperparathyroidism and excessive vitamin D supplementation.
Nathan Goodyear

The Mediterranean diet improves hepatic steatosis and insulin sensitivity in individual... - 0 views

www.sciencedirect.com/...S0168827813001347

NAFLD nutrition non-alcoholic fatty liver mediterranean diet liver disease fatty liver

shared by Nathan Goodyear on 27 Apr 16 - No Cached
  • Nathan Goodyear on 27 Apr 16
     
    Mediterranean diet reduced insulin resistance and liver steatosis in those with NAFLD.
Nathan Goodyear

Adherence to the Mediterranean diet is associated with the severity of non-al... - 0 views

www.sciencedirect.com/...S0261561413002380

mediterranean diet nutrition NAFLD fatty liver insulin resistance liver disease non-alcoholic fatty liver

shared by Nathan Goodyear on 27 Apr 16 - No Cached
  • Nathan Goodyear on 27 Apr 16
     
    In those with NAFLD, mediterranean diet associated with reduced insulin resistance and reduced severity of liver disease; it did not resolve NAFLD
Nathan Goodyear

Study of curcumin on microvasculature characteristic in diabetic rat's liver as reveale... - 0 views

www.ncbi.nlm.nih.gov/...22934459

curcumin curcuma longa turmeric liver liver enzymes liver disease diabetes

shared by Nathan Goodyear on 06 Jul 16 - No Cached
  • Nathan Goodyear on 06 Jul 16
     
    Curcumin at 200 mg/kg found to aid liver repair, regeneration in animal study of diabetes.
Nathan Goodyear

Plasma Adiponectin in Nonalcoholic Fatty Liver Is Related to Hepatic Insulin Resistance... - 0 views

jcem.endojournals.org/...3498.short

NAFLD non-alcoholic fatty liver fatty liver insulin resistance fat IR obesity weight-loss

shared by Nathan Goodyear on 09 Jan 12 - No Cached
  • Nathan Goodyear on 09 Jan 12
     
    in those with nonalcoholic fatty liver disease, low adiponectin is associated with the insulin resistance, not the NAFLD.  But of course, insulin resistance leads to NAFLD
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