Adiponectin increases AMPK activity in skeletal muscle [188, 189] and the liver [189] by promoting Thr172 phosphorylation, likely in response to an increase in the AMP to ATP ratio [189]. Similarly, α-adrenergic signaling increases AMPK activity in skeletal [190] and cardiac muscle [191], and β-adrenergic signaling increases AMPK activity in adipose [192, 193], all through promotion of Thr172 phosphorylation. While activation through β-adrenergic signaling appears to involve the AMP to ATP ratio [192], α-adrenergic signaling appears to work independently of AMP and ATP [190]. Increases in adiponectin have been observed during ketogenic or low-carbohydrate diets, although primarily in obese individuals [194–196]. BHB induces adiponectin secretion in adipocytes [197], indicating that the level of nutritional ketosis may be an important determinant of the extent to which ketogenic diets influence AMPK activity through adiponectin. In regard to catecholamines, epinephrine increases during fasting, and this appears to be dependent on carbohydrate restriction [198], implying that epinephrine is likely to be elevated during nutritional ketosis. Consistent with this, dietary carbohydrate restriction increases catecholamines at rest [155, 199] and in response to exercise [155, 199–202]. This may be, at least in part, a result of glycogen depletion [200, 203], suggesting both direct and indirect effects of glycogen on AMPK activity. The potential for nutritional ketosis to increase catecholamines is further supported by the dependency of the antiseizure effects of ketogenic diets on norepinephrine [204].

Pizza for breakfast? You betchya! This recipe by All Day I Dream About Food slashes carbs by subbing in cauliflower for the standard wheat flour crust, and racks up plenty of fats and protein with toppings like cheese, sausage, eggs, and avocado. It’s as gooey and crispy as your favorite pizza pie, but costs you a slim 5.43 grams of net carbs a serving. Perfect for relaxing weekend mornings or keto-friendly brunch.

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.
309. Lemieux K., Konrad D., Klip A., Marette A. The AMP-activated protein kinase activator AICAR does not induce GLUT4 translocation to transverse tubules but stimulates glucose uptake and p38 mitogen-activated protein kinases alpha and beta in skeletal muscle. FASEB Journal. 2003;17(12):1658–1665. doi: 10.1096/fj.02-1125com. [PubMed] [CrossRef] [Google Scholar]
Hello from Jakarta, Indonesia! I just tried your recipe coz i was making an eggs bennedict & needed something for “bread”. Your recipe was BY FAR the easiest to make & quite tasty! Initially i was worried about the “eggy” taste, but didn’t happen. I think i will be making this often… i will pre-measure the 30gr of almond flour & cut up 10gr of butter pieces for easier assembly in the mornings. Cheers!
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In order to best investigate the efficiency of different fuels, one needs a closed system, where the substrate conditions can be changed and the oxygen consumption and work done can be accurately measured. Isolated (ex-vivo) animal hearts are the best model to study these variables, as it is easy to manipulate the fuel provided (i.e glucose, ketones), to measure the oxygen use and also the amount of work (how much fluid is pumped). 

In skeletal muscle, oxidative capacity and mitochondrial content are related to fiber type. Compared to type II fibers, type I fibers have larger mitochondria [370] with greater oxidative enzyme content [371]. While fiber type is plastic, particularly in response to endurance exercise, transformation from oxidative, slow-twitch fibers (type I) to glycolytic, fast-twitch fibers (type II) is unlikely to occur [372, 373]. Type II fibers, however, can shift in humans from highly glycolytic (type IIx) to more oxidative (type IIa) [373]. Compared to type IIx fibers, type IIa fibers have greater citrate synthase activity, indicating greater mitochondrial content [374]. The relevance of oxidative capacity and fiber type to oxidative stress has been demonstrated by greater mitochondrial respiration with less H2O2 production in permeabilized fibers from rat muscle consisting primarily of type I or IIa fibers versus type IIb fibers [375]. Although muscle fiber-type transformation has been well characterized in response to exercise, this appears to not be the case for ketogenic diets. However, in rats, β-hydroxyacyl-CoA dehydrogenase (β-HAD) has been shown to increase most prominently in glycolytic, type IIb fibers following 4 weeks of a ketogenic diet (% energy: 70 fat, 6 carbohydrate, and 24 protein) [165], suggesting transition of these fibers towards type IIa fibers and, in turn, indicating potential for nutritional ketosis to promote a more oxidative muscle fiber composition.
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