Had to share this for all of you looking for a summary of Brents research on fructose metabolism and its negative affects. He didnt want to post it.... but i did so here you go :-)
Metabolic Disturbances of Fructose Consumption
by Brent Thompson (aka Freak)
I chose the topic of fructose metabolism because it has many negative and far reaching effects on the general public especially those diagnosed with diabetes mellitus. Further, many in the healthcare community often recommend fructose due to its noninsulinergenic properties and it should be done with caution. The glycemic index has given many practitioners and patients a misguided approach to glucose control in my opinion as it is not taking into account the amount of carbohydrates (glucose load), nor the type of carbohydrate and its downstream metabolic effects on the entire body outside the narrow focus of insulin secretion.
As a future diabetes educator I believe it is important to think critically in regards to every aspect of diabetes management even if it is outside current recommendations because more information will lead to tighter control and a better understanding of the disease and methods to prevent complications. Research about fructose metabolism will enhance my professional career because I will be better prepared to serve my clients affected with diabetes and hopefully in public education seminars help people prevent the diagnosis of diabetes by stressing the importance of thoughtful dietary considerations. In my research I have been in communication with several professors who teach nutrition and my findings have changed the way they teach their students about fructose so I have already used my research to help others.
Fructose metabolism occurs almost exclusively in the liver because of the high concentration of GLUT5 (fructose transporter). GLUT5 has a high affinity to transport fructose and a very low affinity to transport glucose. GLUT5 transporters are present almost exclusively in the liver. In tissues where it is present it has such a low affinity for glucose that its action is negligible and is usually never mentioned in most texts. Fructose enters the liver via the portal vein, transported across the cell membrane by GLUT5 and is then phosphorylated (trapped in the liver) by fructokinase into fructose 1 phosphate (F1P). Next the enzyme aldolase B hydrolyzes F1P into glyceraldehyde and dihydroxyacetone phosphate. At this point the end result can be the glycerol portion of a triglyceride or end up as acetyl CoA. Further details are beyond the scope of this summary. The main problems with fructose metabolism are that GLUT5 are expressed almost exclusively in the liver so it fills quickly and has a limited capacity(approximately 75-100g). The other issue is that fructose bypasses the main regulatory step of glycolysis skipping the phosphofructokinase (PFK1) enzyme. In short, fructose is quickly and efficiently converted to triglycerides and acetyl CoA and very little glucose is yielded from fructose ingestion.
Fructose raises triglycerides and VLDL which not only have cardiovascular implications but increasing triglycerides and acetyl CoA leads to adipose tissue deposition and as a result; decreased pretranslational depletion of mRNA for GLUT4 receptors occurs which is directly linked to the amount of adiposity. The decreasing levels of GLUT4 insulin receptors as adipose tissue increases results in poor glucose control and hyperinsulinmemia which increases stress on beta cells effectively leading to premature beta cell dysfunction.
Fructose is also tied to non alcoholic fatty liver disease and metabolic syndrome. Due to the fact that fructose is noninsulinergic fructose by itself does not raise leptin nor does it suppress ghrelin which leads to overeating and no increase in metabolic rate which also results in weight gain.
Fructose causes increased AMP (adenosine monophosphate) deaminase which results in an increase in uric acid and an increased blood pressure. Also, increased uric acid causes insulin resistance independent but additive to that of increased adiposity by depleting nitric oxide and increased oxidative stress. GLUT2 and GLUT5 upregulate themselves; meaning increased fructose causes an increased number of GLUT2 and GLUT5 transporters and as a result increase the intestinal (GLUT2) and liver (GLUT5)ability to process fructose which only adds to the problem.
In closing I want to stress that fruits and vegetables should still be eaten but it is my hope that people will choose foods that do not contain HFCS (high fructose corn syrup). In a world where everything seems processed and containing HFCS if one must consume HFCS please be mindful of the amount. Even small amounts of HFCS over the course of a day can add up to a significant amount.
__________________
Ephesians 6:10-18 | 
