The Carb-Sane Asylum

Below is a wonderfully simple depiction of the mitochondria that depicts one of the points I've been trying to raise above the current internet noise about mitochondrial dysfunction.  That being that when it comes to carb burning (glycolysis) the initial steps occur outside the mitos while fat burning (ß-oxidation) occurs within the mitos.  However both create Acetyl-CoA, and from that point on, metabolism and energy production is the same.  

The detractors of energy balance theory often say something along the lines that thermodynamics goes out the window in living organisms, the rules don't apply.  Nope.  The existence of the Second Law does not violate the First Law! This simply isn't true, and those who say similar must simply not understand these fields.  Humans are not bomb calorimeters or Carnot cycle/combustion engines .  When Dr. Eades tried to discredit Anthony Colpo a while back, he and his compadre Feinman waxed poetic and evoked nightmares of steam tables in their college thermo courses.

I've held off on posting this for a while because it's a screen shot and I have no idea whom to credit. But, since the metabolic pathways are common knowledge, I've decided there's no real harm done "publishing" any depiction of them on my li'l old blog. (If anyone recognizes the graphic, please notify me so I can extend credit) An enduring point of controversy exists in the LC community over higher protein intake vs. higher fat. My personal experience is that the former works for me, but there are plenty of folks doing well on high fat controlled protein approaches. One of the advocates of lower protein intake is Dr. Bernstein the diabetes specialist. Most that advocate his approach agree with his central premise that excess protein is converted to sugar or metabolized as such. While theoretically possible, I've been doing some "re-educating" of myself where protein metabolism, specifically what becomes of any excess is concerned. ...

Acetoacetate and β-hydroxybutyrate in combination with other metabolites release insulin from INS-1 cells and provide clues about pathways in insulin secretion Putting this here for my own orgnization Conclusions: The synergistic insulin release by compounds that can be metabolized to mitochondrial acetyl-CoA, such as KIC, β-hydroxybutyra te, or acetoacetate, in combination with methyl succinate that can be metabolized to mitochondrial oxaloacetate, suggests that acetyl-CoA and oxaloacetate condense in the citrate synthase reaction to form citrate. Numerous compounds can be formed from citrate, and citrate can carry acetyl-CoA and oxaloacetate out of the mitochondria to the cytosol. Many compounds, including most short-chain acyl-CoAs, can be formed from acetyl-CoA in the cytosol. KIC and β-hydroxybutyra te can also be directly converted to acetoacetate and acetyl-CoA in the mitochondria. Acetoacetate can be exported to the cytosol and converted to acetoacetyl-CoA to...