The occurrence of mitohormesis is further supported by the potential for mtROS to simultaneously induce bioenergetic and antioxidant adaptations through a single signaling mediator. As discussed later in this review, this mediator is the transcription factor peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), and its role in simultaneously inducing bioenergetic and antioxidant adaptations has been demonstrated in several experimental models of mtROS production, including treatments with paraquat and H2O2. Paraquat is an herbicide that is reduced by the mtETC and subsequently initiates mtROS production by reacting with O2 to produce O2•− [74, 75], and H2O2 is a common form of mtROS. Treatment of a fibroblast cell line (10T1/2) with H2O2 has induced expression of both antioxidant enzymes (SOD1, SOD2, and GPx1) and proteins involved in mitochondrial oxidative phosphorylation, all in a manner largely dependent on PGC-1α [76]. Demonstrating the hormetic benefit of this response in a variety of brain cells, overexpression of PGC-1α protected against cell death induced by H2O2 or paraquat treatment, and this occurred in conjunction with changes in gene expression similar to those observed with the 10T1/2 cells [76]. Although the central role of PGC-1α in linking mitochondrial bioenergetics with antioxidant defense appears to not have been thoroughly investigated in vivo, some suggestive evidence does exist. In skeletal muscle of mice treated with paraquat, content of proteins involved in mitochondrial oxidative phosphorylation and uncoupling have been found to increase in conjunction with greater nuclear localization of PGC-1α [77]. Traditional antioxidant proteins were not measured, but, as will be discussed later, the increase in uncoupling proteins can be regarded as an indication of enhanced antioxidant defense based on the potential of these proteins to decrease mtROS production.
Nutritional ketosis may facilitate PGC-1α activity through multiple mechanisms. Since PGC-1α is activated by AMPK and SIRT1, nutritional ketosis may initiate PGC-1α activity through these enzymes. As previously mentioned, catecholamines and adiponectin facilitate PGC-1α activity by promoting its expression, and insulin inhibits PGC-1α through downstream phosphorylation, all independent of AMPK. As previously discussed, a ketogenic diet may increase catecholamines and adiponectin and is well known to decrease insulin, indicating that nutritional ketosis may directly facilitate PGC-1α activity through these hormones. Supporting these potential mechanisms, a ketogenic or low-carbohydrate diet has increased expression, protein content, and activation of PGC-1α [149, 231, 317], as well as expression of its target PPARα [87, 148]. Furthermore, in skeletal muscle of mice following a ketogenic diet, the resulting increases in O2 consumption and expression of genes related to fat oxidation appear to be dependent on PGC-1α [157]. Ketones likely contribute to this signaling as well based on the recent observation that the increased hepatic expression of PPARα targets induced by a ketogenic diet did not occur with a nonketogenic low-carbohydrate diet [37].
Cirrhosis of the liver refers to a disease in which normal liver cells are replaced by scar tissue caused by alcohol and viral hepatitis B and C. This disease leads to abnormalities in the liver's ability to handle toxins and blood flow, causing internal bleeding, kidney failure, mental confusion, coma, body fluid accumulation, and frequent infections.
Eating mindfully. A child who learns to see food as fuel and not emotional compensation can start to make better choices at mealtime — for example, selecting complex carbs instead of simple carbs (whole-grain instead of white bread, brown rice instead of white); getting more fiber with beans, fruits, and vegetables; choosing "healthy" fats like olive oil and nuts; and avoiding too many empty calories from soda and sweets.
Proof the yeast. This involves mixing dry active yeast with water that’s just warm to touch (between 105-110°F to be precise) and maple syrup or honey for 7 minutes until foamy. And before you scream sugar (!!) remember that the yeast will feed on such sugar to emit carbon dioxide, so it doesn’t affect the carb count at all. And yes, this is a scientific fact.
First of all, thanks for the recipe. I tried it yesterday with coconut flour and egg whites, and I failed miserably. It rose 5 or 6 times in volume and then collapsed like the world economy. Also, it was very moist on the inside. I’ll try the almond flour version with half the baking powder and full eggs this time, but I’m having trouble wrapping my head around measurements. If 1 and 1/2 cup of almond flour is 5oz, how can 1/2 cup of coconut flour be 2.5oz (equalling 7.5oz for 1 and 1/2 cup)? If anything, almond flour is more dense, not less.
Ketogenic diets (around 50 grams of carbs per day) are extremely effective for getting lean because you reset the body’s enzymatic machinery to use fat as its primary fuel source in the absence of carbs. I see three problems with your diet that are certainly causing your fat-loss plateau—too much protein, not enough good fat, and residual carbohydrates.
In low carb and keto baking, we’re concerned with two things: 1) keeping carbs low, and 2) still achieving a baked good that has great flavor and texture (because if we can’t gag it down there’s just no point, right? Lol). Low carb bread recipes are usually gluten free and grain free (although we’ve seen a couple that use oat fiber), but then the challenge is to get creative to get the right combination of ingredients to yield something that rises properly and tastes good.
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