The Carb-Sane Asylum

NEFA = Non-Esterified Fatty Acids aka Free Fatty Acids (FFA) (By the way, I've just always preferred the NEFA acronym because in my head it sounds out more nicely than "ef ef ay" -- and for whatever reason, I sound it out "knee fah", though a reader once wondered about "neh fay".  I don't know there's a correct pronunciation for acronyms like this!) On a hypothetical Metabolic SAT test NEFA are to lipids what glucose is to carbohydrates and amino acids are to proteins.  These are the forms of the three macronutrient classes that are absorbed/transported into and out of cells and circulation and the forms that enter into the energy-producing pathways.  By contrast, lipids are stored as triglycerides (aka triacyl glycerols, TAG), while carbs are stored in rather more limited quantities as glycogen, and there exists essentially no true storage depot for protein in excess of "tissue maintenance" needs.

Caffeine and Insulin Sensitivity   (full text PDF free till end of the month) A number of reports have observed that acute caffeine ingestion decreases glucose tolerance and insulin sensitivity, and have raised the question whether its increased consumption throughout the world in the form of coffee and cola beverages might be of public health concern in the development of type 2 diabetes. Although some epidemiologic studies have found strong associations between coffee intake and detrimental lifestyle factors that favor obesity and diabetes, it is interesting that in spite of this, they have demonstrated that increased coffee consumption is associated with a decreased risk of developing type 2 diabetes.   When lifestyle confounders are taken into account, individuals consuming 6 cups coffee per day have at least 50% less risk of developing type 2 diabetes than those consuming 2 cups per day . Although it is perhaps premature to rec...

This post may well make heads spin.  It sure did mine. A common claim in LC circles is that we "waste" excess fats through futile cycling.  Although this has not been demonstrated in any significant amount in humans except in massive fat overfeeding, it is still incorporated into books and blog posts by the likes of Dr. Mike Eades (futile cycling to "blow off" low carb excesses is stated as if fact in The 6 Week Cure). Inherent in these statements is the implication that this only happens for excess dietary fat when carbs are low ... insulin would be trapping the fats in the cells as the theories go.  Well ... Substrate cycling between de novo lipogenesis and lipid oxidation: a thermogenic mechanism against skeletal muscle lipotoxicity and glucolipotoxicity   (2004 Review Article,  PDF)

Reader Ryan emailed me this link a while back and I've been remiss in getting around to it.  Better late than never!  Thanks for the link Ryan! Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans Mitochondrial dysfunction and oxidative stress have been implicated in the disease process, but the underlying mechanisms are still unknown. Here we show that in skeletal muscle of both rodents and humans, a diet high in fat increases the H 2 O 2 -emitting potential of mitochondria, shifts the cellular redox environment to a more oxidized state, and decreases the redox-buffering capacity in the absence of any change in mitochondrial respiratory function. Furthermore, we show that attenuating mitochondrial H 2 O 2  emission, either by treating rats with a mitochondrial-targeted antioxidant or by genetically engineering the overexpression of catalase in mitochondria of muscle in mice, completely preserves i...

High-fat diet, muscular lipotoxicity and insulin resistance A high dietary fat intake and low physical activity characterize the current Western lifestyle.  Dietary fatty acids do not stimulate their own oxidation and a surplus of fat is stored in white adipose tissue, liver, heart and muscle. In these organs intracellular lipids serve as a rapidly available energy source during, for example, physical activity. However, under conditions of elevated plasma fatty acid levels and high dietary fat intake, conditions implicated in the development of modern diseases such as obesity and type 2 diabetes mellitus, fat accumulation in liver and muscle (intramyocellular lipids; IMCL) is associated with the development of insulin resistance. Recent data suggest that IMCL are specifically harmful when combined with reduced mitochondrial function, both conditions that characterize type 2 diabetes. In the (pre)diabetic state reduced expression of the tra...

Elevated Concentrations of Nonesterified Fatty Acids Increase Monocyte Expression of CD11b and Adhesion to Endothelial Cells First, a layperson friendly description of Monocytes : Monocytes are a type of leukocyte or white blood cell which play a role in immune system function. Depending on a patient's level of health, monocytes make up between one and three percent of the total white blood cells in the body. They can be counted as part of a blood test, and changes in their levels can indicate changes in a patient's health. As a general rule, a low monocyte count is a good sign, and a high count indicates that a problem is present... ... Levels of monocytes in the blood tend to rise when someone has an infection, because more of these cells are needed to fight it. Monocytes can also increase in response to stress and other factors. A high monocyte count may be referred to as monocytosis, and it is typically addressed by determining why the count is so high, and addressing th...

Fructose and Tagatose Protect Against Oxidative Cell Injury by Iron Chelation Abstract To further investigate the mechanism by which fructose affords protection against oxidative cell injury , cultured rat hepatocytes were exposed to cocaine (300 ) or nitrofurantoin (400 ). Both drugs elicited massively increased lactate dehydrogenase release. The addition of the ketohexoses -fructose (metabolized via glycolysis) or -tagatose (poor glycolytic substrate) significantly attenuated cocaine- and nitrofurantoin- induced cell injury, although both fructose and tagatose caused a rapid depletion of ATP and compromised the cellular energy charge. Furthermore, fructose, tagatose, and sorbose all inhibited in a concentration-d ependent manner (0–16 mM) luminol-enhance d chemiluminescen ce (CL) in cell homogenates, indicating that these compounds inhibit the iron-dependent reactive oxygen species (ROS)-mediated peroxidation of luminol. Indeed, both Fe 2+ and Fe 3+ further increased cocaine...