Excerpts From “Ketogenic diet for obesity: friend or foe?”

The following are excerpts from Resource (1), Ketogenic diet for obesity: friend or foe? :

2. Ketogenic Diets in the Clinic

Even though the ketogenic diet may be useful as part of the treatment of various diseases (see Paoli et al. [11]), especially in pediatric pharmacoresistant epilepsy [12], the more common
situation for the general practitioner is the use of KD by patients in order to lose weight. KDs have undoubtedly been shown to be effective, at least in the short to medium term, as a tool to fight
obesity [13], hyperlipidemia and some cardiovascular risk factors [14–16], but ketogenic diets also raise some concerns among physicians [17]. Many of the concerns about the use of ketogenic diet as therapeutic tools could be attributed to a broad lack of knowledge about the physiological mechanisms
involved. Ketogenic diets induce a metabolic condition named “physiological ketosis” by Hans Krebs, to distinguish it from the pathological diabetic ketosis [18].

3. The Physiology of Ketosis

After a few days of fasting or a drastically reduced carbohydrate diet (below 20 g per day), the body’s glucose reserves become insufficient for the production of oxaloacetate for normal fat oxidation in the Krebs cycle and for the supply of glucose to the central nervous system (CNS) [19–22]. Regarding the first issue, oxaloacetate is relatively unstable at body temperature, thus it is necessary (a minimal amount of oxaloacetate is required for an optimal functioning of the Krebs cycle) to supply the tricarboxylic acid cycle with oxaloacetate derived from glucose through ATP dependent carboxylation of pyruvic acid by pyruvate carboxylase [23].

Regarding the second issue, the CNS cannot use fatty acids as an energy source (because they do not cross the blood-brain barrier), thus glucose is ordinarily the sole fuel for the human brain [24]. After 3–4 days of fasting or a very low carbohydrate diet the CNS needs an alternative energy source [19–22] and this is derived from the overproduction of acetyl-CoA which leads to the production of so-called ketone bodies (KB): acetoacetate (AcAc), β-hydroxybutyric acid (BHB) and acetone (Figures 1 and 2). This process is called ketogenesis and occurs principally in the mitochondrial matrix in the liver [25]. It is important to underline that the liver produces ketone bodies, but is unable to utilize them because the absence of the enzyme 3-ketoacyl CoA transferase required to convert acetoacetate into acetoacetyl-CoA.

Resources:

(1) Ketogenic diet for obesity: friend or foe? [PubMed Abstract] [Full Text HTML] [Full Text PDF]. Int J Environ Res Public Health. 2014 Feb 19;11(2):2092-107. doi: 10.3390/ijerph110202092.

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