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Nathan Goodyear

The Journal of Bone & Joint Surgery | Article - 0 views

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    It is no surprise that hyperglycemia is associated with increased hospital stay and post operative infection.  I have seen this in my former population.  Especially in prolapse and incontinence surgeries (which I no longer perform).  However, what is interesting is that 1/3 of the non-diabetics are hyperglycemic.  The preparation of the individual has just as much to do with the successful outcome of the surgery as does the surgery itself.
Nathan Goodyear

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

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    insulin potentiates NF-kappaB-dependent transcriptional activity induced by hyperglycemia
Nathan Goodyear

The Antihyperglycemic Drug α-Lipoic Acid Stimulates Glucose Uptake via Both G... - 0 views

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    Alpha lipoic acid aids insulin action of glucose uptake through its GLUT4 activation.  ALA aids diabetes and other states of hyperglycemia.
Nathan Goodyear

Ketone supplementation decreases tumor cell viability and prolongs survival of mice wit... - 0 views

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    animal study finds that high glycemic diets increase risk of cancer, hyperglycemia = poor prognosis in those diagnosed with cancer, blood glucose levels correlated to tumor growth, ketogenc diet lowers glucose, insulin, IGF=1, and ketones directly inhibit tumor growth!!  So what is the cancer community waiting for?
Nathan Goodyear

Androgen deprivation therapy in men with prostate cancer: how should the side effects b... - 0 views

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    Androgen deprivation therapy in men has been shown to worsen insulin resistance and precipitate type II Diabetes as well as stimulate weight gain.  This suggests a cause effect relationship between Testosterone and insulin sensitivity.  Other studies have pointed to a reciprocal decline in Testosterone due to hyperglycemia--both acute and chronic.   Androgen deprivation has a significant long list of cardiovascular risks and this should be discussed with the patient.
Nathan Goodyear

Original Articles: Comparison of Insulin Action on Glucose versus Potassium Uptake in H... - 0 views

  • When treating hyperkalemia, insulin remains efficacious in diabetics and nondiabetics and one does not need to resort to b-agonists, and diabetics do not require different doses of insulin to shift potassium
  • the commonly encountered “insulin-resistant” patients actually have preserved insulin-induced potassium disposal, one wonders why their high insulin levels are not causing hypokalemia
  • insulin independently regulates glucose and potassium uptake into cells and this independence explains why in noninsulin-dependent diabetic insulin resistance leads to impaired insulin uptake into cells but has no effect on the cell's potassium disposal
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  • insulin suppresses glycogenolysis, gluconeogenesis, lipolysis and fatty acid release, and protein catabolism and is the principal hormone that stimulates glucose uptake into mainly skeletal muscle and to a certain extent adipocytes
  • Plasma [K+] is a major determinant of the resting potential of all cells
  • Hyperkalemia and hypokalemia are silent yet fatal disturbances because of their arrhythmogenic potentials
  • Basal insulin maintains fasting plasma [K+] within the normal range
  • When insulin levels are suppressed, plasma [K+] rises and pronounced hyperkalemia develops after a potassium load
  • Potassium is a well proven insulin secretagogue
  • Insulin is a key defender against exogenous potassium load by using intracellular buffering to minimize hyperkalemia before renal excretion
  • Hyperkalemia is often encountered in patients with diabetes
  • The insulin-deficient state in type 1 diabetes predisposes to hyperkalemia because of an impaired ability of potassium to enter cells. During hyperglycemic hypertonic states in type 1 and type 2 diabetics, potassium is carried out of cells by convective flux as the most abundant intracellular cation
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    good review of the potassium, glucose, insulin relationship mostly in diabetes.  In diabetes, hyperkalemia is present due to the hyperglycemia and the associated exchange.  Inuslin independantly regulates potassium and glucose intake into the cell.  INterestingly, in IR found in diabetes, the hyperkalemia is the norm, which should cause hypokalemia--the authors were perplexed by this finding.
Nathan Goodyear

Increased muscular dehydroepiandrosterone levels are associated with improved hyperglyc... - 0 views

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    Exercise, DHEA, and DHT increased GLUT4 uptake of glucose, increasing glycemic control.
Nathan Goodyear

Glucose and insulin components of the metabol... [Am J Epidemiol. 2004] - PubMed - NCBI - 0 views

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    Correlation between increasing male hormones (androgens) and poor glucose control and metabolic syndrome in post menopause women.
Nathan Goodyear

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

  • 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
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  • 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
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    great review of cirrhosis and BCCA supplementation.
Nathan Goodyear

Long-Term Glycemic Control Influences the Long-Lasting Effect of Hyperglycemia on Endot... - 0 views

  • Combining insulin and vitamin C, however, normalized endothelial dysfunction and nitrotyrosine.
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    Vitamin C normalized vascular dysfunction found in Diabetes
Nathan Goodyear

Homeostasis in Intestinal Epithelium Is Orchestrated by the Circadian Clock and Microbi... - 0 views

  • a lack of microbiota results in a permanent ileal overproduction of corticosterone due to decreased expression of the D-box-binding E4BP4 repressor. This hypercorticosterolism generates systemic metabolic defects (hyperglycemia, insulin resistance, increased TG and FA)
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    to be read article on the communication between gut microbiota and intestinal epithelial cells and the resultant metabolic impact.
Nathan Goodyear

Nutrients | Free Full-Text | Effect of Probiotics on Metabolic Outcomes in Pregnant Wom... - 0 views

  • The gut microbial composition is altered during pregnancy
  • probiotic supplements may contribute to the maintenance of bacterial diversity and glucose homeostasis in individuals with metabolic disturbances
  • Assessment of four randomized controlled trials in this review involving 288 pregnant women with GDM found that a 6–8 week probiotic intervention did not improve FBG or LDL-cholesterol levels
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  • probiotic supplementation in women with GDM was associated with significant reductions in insulin resistance
  • One proposed method is by the production of short chain fatty acids (SCFAs), generated as a by-product of bacterial fermentation of dietary fibers. SCFAs act as an energy source for intestinal cells and have been found to regulate the production of hormones effecting energy intake and expenditure such as leptin and grehlin
  • Another hypothesized mechanism of SCFA action includes reducing gastrointestinal permeability by upregulating transcription of tight junction proteins, enhancing production of Glucagon-like peptide-2 (GLP-2) which promotes crypt cell proliferation, and reducing inflammation in colonic epithelial cells by increasing PPAR-gamma activation
  • Maintenance of the integrity of the gut barrier minimizes the concentration of lipopolysaccharide (LPS) in circulation
  • LPS is a structural component of gram negative bacterial cell walls, which induces an immune-cell response upon absorption into the human bloodstream, stimulating proinflammatory cytokine production and the onset of insulin resistance and hyperglycemia
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    Review (4 studies) found that 6-8 weeks of probiotic therapy of pregnant women with gestational diabetes improved insulin resistance.
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