Metabolic syndrome is a serious health condition that affects about 23 percent of adults and places them at higher risk of cardiovascular disease, diabetes, stroke and diseases related to fatty buildups in artery walls. The underlying causes of metabolic syndrome include overweight and obesity, physical inactivity, genetic factors and getting older.
Ketogenesis is the pathway that forms ketone bodies from fatty acids. Starvation (specifically low levels of blood insulin and glucose) triggers ketogenesis in the liver cells’ mitochondria. Two molecules of acetyl-CoA from the breakdown of fatty acids are condensed via acetyl-CoA transferase to form acetoacetyl-CoA; a third is added to form 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) in a reaction catalysed by HMG-CoA synthase. HMG-CoA lyase then splits this to re-generate acetyl-CoA and form one molecule of AcAc. Beta-hydroxybutyrate (BHB) is formed from reduction of AcAc by BHB-dehydrogenase enzyme, and acetone results from spontaneous, non-enzymatic decarboxylation of AcAc. Acetone is a volatile molecule which is primarily excreted in the breath, although some evidence suggests that a small amount can be metabolised and oxidised4.

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Our bodies need sugar to make energy for the cells. Without it, we cannot do basic functions. When we eat foods with glucose, insulin pairs with it to allow it to enter into the cell wall. If the insulin is not there, then the glucose molecule can’t get through the wall and cannot be used. The extra glucose hangs out in the bloodstream which is literally high blood sugar.
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Ketogenic and low-carbohydrate diets greatly increase reliance on fat oxidation [78–89], which would logically be expected to increase mitochondrial respiration and mtROS production and, in turn, induce mitohormesis. Furthermore, mtROS produced through RET appears to have particular relevance to hormetic adaptation, including increased lifespan [90]. Nutritional ketosis is likely to increase RET by altering the FADH2 to NADH ratio. As the primary source of acetyl CoA shifts from glycolysis to β-oxidation and ketolysis, this ratio increases, more than doubling for β-oxidation of longer-chain fatty acids. Electrons from FADH2 reduce the CoQ pool through complex II and ETF-QO, thereby increasing RET [91, 92]. This induction of RET by alteration of substrate availability can also be influenced by configuration of mtETC complexes into supercomplexes [90]. The greater potential for mtROS production through RET is consistent with evidence of mitochondria producing more H2O2 during oxidation of palmitoyl carnitine versus pyruvate [93, 94]. Furthermore, succinate is generated during ketolysis by succinyl-CoA:3-oxoacid CoA-transferase (SCOT), which also promotes RET by reducing the CoQ pool through complex II. Demonstrating the likely role of RET in mitohormesis, particularly within the context of nutritional ketosis, extension of lifespan in C. elegans through BHB treatment is dependent on both complex I function and expression of bioenergetic and antioxidant proteins [95].

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