Points of Interest – “Fructose, Insulin Resistance, and Metabolic Dyslipidemia”

Below are some key points of interest I’ve noted with respect to the article entitled “Fructose, Insulin Resistance, and Metabolic Dyslipidemia”

  • A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism.
  • The epidemic of type 2 diabetes is complicated by the fact that it is a multi-factorial disease, frequently associated with a cluster of pathologies including obesity, hypertriglyceridemia, impaired glucose tolerance, and insulin resistance, collectively referred to as the metabolic syndrome (formerly known as syndrome X and insulin resistance syndrome)

  • Recently, the National Cholesterol Education Panel (NCEP) has officially described and identified a number of risk factors for cardiovascular diseases. These include: 1) abdominal obesity, 2) elevated TG levels, 3) low high density lipoprotein (HDL)-cholesterol levels, 4) increased blood pressure, and 5) impaired fasting glucose
  • The use of HFCS (High Fructose Corn Syrup) has increased an alarming 1000% between 1970 and 1990. In 1970, individual consumption of fructose was only 0.5 lb/year. However, in 1997, this figure rose to an alarming 62.4 lb/year
  • The exposure of the liver to such large quantities of fructose leads to rapid stimulation of lipogenesis and TG accumulation, which in turn contributes to reduced insulin sensitivity and hepatic insulin resistance/glucose intolerance.
  • Studies involving commonly consumed fruit juices showed that natural fructose carbohydrates can alter lipid and protein oxidation biomarkers in the blood, and mediate oxidative stress responses in vivo
  • Fructose can uncontrollably produce glucose, glycogen, lactate, and pyruvate, providing both the glycerol and acyl portions of acyl-glycerol molecules. These particular substrates, and the resultant excess energy flux due to unregulated fructose metabolism, will promote the over-production of TG (triglycerides)
  • The insulin sensitizer agonist, peroxisome proliferator-activated receptor-gamma, stimulates adiponectin production and adiponectin is in fact thought to be part of this agonist’s mechanism lowering circulating fatty acids and increasing fat oxidation. The net effect is to decrease liver TG and increase insulin sensitivity. Chronic fructose consumption reduces adiponectin responses, contributing to insulin resistance.
  • In 1986, Levine et al. found that fructose, administered in the form of the disaccharide sucrose, promotes obesity more than glucose because fructose does not stimulate thermogenesis
  • Glucose stimulates both TG production, and TG removal, maintaining homeostasis. Fructose stimulates TG production, but impairs removal, creating the known dyslipidemic profile

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