Based on the reciprocal activation described above, nutritional ketosis is likely to activate SIRT1 and SIRT3 indirectly through activation of AMPK. However, more direct activation of sirtuins by nutritional ketosis is possible. Since reduction of NAD+ to NADH occurs outside of mitochondria only during glycolysis, which is less active during nutritional ketosis, more cytosolic NAD+ remains oxidized, further facilitating activation of SIRT1 . In addition to the decrease in glucose availability during nutritional ketosis, glycolysis may be further inhibited through activation of pyruvate dehydrogenase kinase and subsequent inhibition of pyruvate dehydrogenase (PDH), which occurs in response to dietary carbohydrate restriction [248–251] or infusion of BHB, ACA, or fatty acids . Consistent with the relevance of these factors to nutritional ketosis, a ketogenic diet (% energy: 89 fat, <1 carbohydrate, and 10 protein) has decreased expression of PDH in mouse liver . More importantly, there is direct evidence of nutritional ketosis promoting an increase in NAD+ concentration. Treatment with BHB + ACA (1 mM each) has increased NADH oxidation in rat neocortical mitochondria , and a ketogenic diet (Bio-Serv F3666) has increased NAD+ concentration in rat hippocampus . There is also evidence of nutritional ketosis regulating sirtuin expression. A low-carbohydrate (20% of energy) diet combined with ketone esters (6% w/v) has increased SIRT1 protein content in brown adipose of mice , and a ketogenic diet (% energy: 90 fat, 0 carbohydrate, and 10 protein) has increased SIRT3 expression in mouse liver .
If there’s one thing keto dieters miss when they're trying to enjoy brunch, it’s those damn roasted potatoes. Yet you can dig into these "potatoes"—a.k.a. turnips—by Cast Iron Keto. They have so much flavor from paprika, garlic powder, salt, and pepper and only 4 grams of net carbs—you won’t even miss the real thing. Pair with eggs, fish, or meat for extra protein, and you’re set. (Though there is some bacon already!)
As a matter of fact, in animal models intracerebroventricular injections of long-chain FA reduced hypothalamic expression of NPY. NPY is an important orexogenic neuropeptide that is a downstream target of leptin and insulin in the hypothalamus. In some forms of hyperphagic obesity, characterized by elevated plasma leptin and insulin levels, the lack of action of insulin on NPY expression could explain the pathological condition. Central administration of oleic acid, fatty-acid synthase, or CPT-1 inhibitors prevents the rise in hypothalamic NPY mRNA induced by fasting (Obici et al., 2003). But glucose level is also involved in KD's food control mechanisms. According to glucostatic theory (Mayer, 1955) data indicates that ketosis did not influence FA glucose but instead stimulated the elevation of post-prandial glucose (Sumithran and Proietto, 2013) in non-diabetic subjects, while in diabetics there was a reduction of fasting glucose (Westman et al., 2008). It is important to note that carbohydrate availability may increase cellular levels of long-chain FA-CoA through an increase of malonyl-CoA, which inhibits oxidation of FAs.
Thanks for starting a new recipe since the comments were getting out of hand on the sub rolls post 🙂 Can you say what size loaf pan you used for this. I have tried the recipe twice in a loaf pan of 2 very different sizes, and they turned out radically different. I think there is a sweet spot which you obviously found with yours. I’d like to find it for mine, too. Thanks for the great bread recipe. It’s one of the only recipes I know by heart because it is so elegantly simple.
Would highly recommend listening to Tim Noakes and his trail in Cape Town – he was pretty much the trigger for me to switch to LCHF and now I am starting to educate myself on what I need to follow a path that works for me. The information on Verta is giving me more information to enable me to ask my Dr for what I want – I know this will be an uphill battle and this information will help me avoid getting railroaded into the so called norms. It also give the Dr a way out because then I am asking him to help me go down a certain path that he is not responsible for recommending if it bucks the system.
This is a classic breakfast for a reason: It's delicious, and the steak and eggs each pack a monster punch of protein to keep you fueled up till lunch. Next time you're grilling up steak at night, cook a little extra with incredible keto breakfast leftovers in mind. Tasteaholic's take uses sirloin, a leaner cut of beef, but feel free to use what you have on hand.
Hunger and satiety are two important mechanisms involved in body weight regulation. Even though humans can regulate food intake by will, there are systems within the central nervous system (CNS) that regulate food intake and energy expenditure. This complex network, whose control center is spread over different brain areas, receives information from adipose tissue, the gastrointestinal tract (GIT), and from blood and peripheral sensory receptors. The actions of the brain's hunger/satiety centers are influenced by nutrients, hormones and other signaling molecules. Ketone bodies are the major source of energy in the periods of fasting and/or carbohydrate shortage and might play a role in food intake control.