Also see:
Aldosterone, Sodium Deficiency, and Insulin Resistance
Diabetes: Conversion of Alpha-cells into Beta-cells
Free Fatty Acid Suppress Cellular Respiration
Women, Estrogen, and Circulating DHA
Insulin Inhibits Lipolysis
The Randle Cycle
Comparison: Carbon Dioxide v. Lactic Acid
Carbon Dioxide Basics
Carbon Dioxide as an Antioxidant
Comparison: Oxidative Metabolism v. Glycolytic Metabolic
Promoters of Efficient v. Inefficient Metabolism
Trauma & Resuscitation: Toxicity of Lactated Ringer’s Solution
Enzyme to Know: Pyruvate Dehydrogenase
Insulin Inhibits Lipolysis
Lactic Acidosis and Diabetes
“Therapeutically, even powerful toxins that block the glycolytic enzymes can improve functions in a variety of organic disturbances “associated with” (caused by) excessive production of lactic acid…But several nontoxic therapies can do the same things: Palmitate (formed from sugar under the influence of thyroid hormone, and found in coconut oil), vitamin B1, biotin, lipoic acid, carbon dioxide, thyroid, naloxone, acetazolamide, for example.” -Ray Peat, PhD
“Thyroid hormone, palmitic acid, and light activate a crucial respiratory enzyme, suppressing the formation of lactic acid. Palmitic acid occurs in coconut oil, and is formed naturally in animal tissues. Unsaturated oils have the opposite effect.” -Ray Peat, PhD
Am J Physiol. 1997 Nov;273(5 Pt 1):C1732-8.
Glycolysis inhibition by palmitate in renal cells cultured in a two-chamber system.
Bolon C, Gauthier C, Simonnet H.
A major shortcoming of renal proximal tubular cells (RPTC) in culture is the gradual modification of their energy metabolism from the oxidative type to the glycolytic type. To test the possible reduction of glycolysis by naturally occurring long-chain fatty acids, RPTC were cultured in a two-chamber system, with albumin-bound palmitate (0.4 mM) added to the basolateral chamber after confluency. Twenty-four hours of contact with palmitate decreased glycolysis by 38% provided that carnitine was present; lactate production was decreased by 38%, and the decrease in glycolysis resulted from a similar decrease of basolateral and apical net uptake of glucose. In contrast to the previously described effect of the nonphysiological oxidative substrate heptanoate, palmitate promoted a long-term decrease in lactate production and sustained excellent cellular growth. After 4 days of contact, decreased glycolysis was maintained even in the absence of carnitine and resulted from a decrease of basolateral uptake only, suggestive of long-term regulation different from the earlier effects. Thus, although cultured RPTC lost their oxidative phenotype, they exhibited a type of regulation (Randle effect) that is found in the oxidative-type but not in the glycolytic-type tissues, therefore unmasking a regulative capacity barely detectable in fresh RPTC. Low PO2 (50 mmHg in the apical chamber) could be a major cause of elevated glycolysis and could hinder the effects of palmitate.
