The concentration of ketone bodies may vary depending on diet, exercise, degree of metabolic adaptation and genetic factors. Ketosis can be induced when a ketogenic diet is followed for more than 3 days. This induced ketosis is sometimes called nutritional ketosis. This table shows the concentrations typically seen under different conditions
Although the hunger-reducing effect of KD is well-documented, its main mechanisms of action are still elusive. The global picture is complicated by the contradictory role of ketosis on anorexigenic and orexigenic signals (summarized in Figure Figure4).4). Ketones (mainly BHB) can act both orexigenically or anorexigenically. In the orexigenic mechanism, it increases the circulating level of adiponectin, increasing brain GABA and AMPK phosphorylation and decreasing brain ROS production. The anorexigenic mechanism triggers a main normal glucose meal response, increasing circulating post-meal FFA (thus reducing cerebral NPY), maintaining CCK meal response and decreasing circulating ghrelin. It can be postulated that the net balance of the contrasting stimuli results in a general reduction of perceived hunger and food intake. More studies are needed to explore the mechanism of potential beneficial effects of KD on food control.
We can say that no species, including humans, could have survived for millions of years without the ability to withstand brief periods of hunger or starvation (Amen-Ra, 2006). These periods of fasting are themselves ketogenic (McCue, 2010) during which the concentrations of insulin and glucose decrease while that of glucagon increases in the attempt to maintain normal blood glucose levels. When the body passes from a condition of food abundance to one of deprivation (or else via VLCKD simulated deprivation), there is, with a slight delay, an increase in the concentration of free FAs as well as KB in the blood. Thus, from this point of view KD could be compared to caloric restriction for fasting. These manipulations of nutrients, both in quantity and quality, seem to not only act on blood glucose/KB level but also to promote changes in metabolic pathways and cellular signaling. How this kind of metabolic condition (ketosis) can affect satiety and hunger mechanisms is still a matter of debate.
My name is Kevin. My life changed when I realized that healthy living is truly a lifelong journey, mainly won by having a well-balanced diet and enjoying adequate exercise. By experimenting in the kitchen and openly sharing my meals, I learned that healthy eating is hardly boring and that by making a few adjustments, I could design a diet that could help me achieve my personal fitness goals. Our bodies are built in the kitchen and sculpted in the gym.
Brain glucose and KB uptake was investigated in rats subjected to mild experimental ketonemia induced by 2 weeks on the KD or by 48 h fasting. To test this, researchers developed a carbon-11 labeled AcAc (11)C-AcAc for PET use. They found in rats that after 10 days of KD (11)C-AcAc brain uptake increased up to 8-fold, an increase comparable to those measured after 48 h of fasting (Pifferi et al., 2008).
Hi Laura, just reading your comment and I feel the need to reply to let you know that ketogenic diets and ketoacidosis are completely different states in the body. If you have indeed read as much as you claim, I’m sure you’re aware that ketosis or a state of burning fat for fuel, is not even similar to a state of ketoacidosis seen mostly in type 1 diabetics.
The main ingredients in this recipe (chicken, cream cheese, cheddar cheese, and bacon) are all part of a low-carb, ketogenic diet. We skipped the store-bought Ranch seasoning mix because it usually contains sugar, quite a bit of salt, and preservatives that we try to avoid if possible. Instead we used a keto-friendly mix of dried chives, garlic powder, onion powder, crushed red pepper flakes, dried dill, salt, and black pepper to season our Crack Chicken.
The process of generation ketones (ketogenesis) is kept in check by the presence of insulin in the body. Insulin regulates the flow of fatty acids from our fat cells, and it acts in a feedback loop to regulate ketogenesis. As long as insulin is circulating within the body, in general, the flow of fatty acids and the production of ketone bodies will be limited to a range that is not dangerous. In contrast, ketoacidosis is a condition associated with a lack of insulin. For example, it can manifest in type 1 diabetics who fail to inject enough insulin, or who are newly diagnosed.
If you're healthy and eating a balanced diet, your body controls how much fat it burns, and you don't normally make or use ketones. But when you cut way back on your calories or carbs, your body will switch to ketosis for energy. It can also happen after exercising for a long time and during pregnancy. For people with uncontrolled diabetes, ketosis is a sign of not using enough insulin.
On the contrary, in the brain, as mentioned above, the increase of AMPK activity leads to higher food intakes. But the effect of AMPK in the brain is more complicated; mice lacking AMPKa2 in pro-opiomelanocortin neurons develop obesity, while the deficiency of AMPKa2 in agouti-related protein neurons results in an age-dependent phenotype. Thus, the conclusion is that even while AMPK is a regulator of hypothalamic functions, it does not act as a signal for energy deficit or excess (Claret et al., 2007). However, the picture is more complex than this (Figure (Figure3);3); BHB induces AgRP expression while increasing ATP and inhibiting AMPK phosphorylation (Cheng et al., 2008). Moreover, Laeger and colleagues have recently demonstrated that under physiological conditions BHB decreases AMPK phosphorylation and AgRP mRNA expression in GT1-7 hypothalamic cells (Laeger et al., 2012).
Following the ketogenic diet and achieving ketosis may be beneficial if you’re living with type 2 diabetes and need to manage your symptoms. Limiting carbohydrate intake is crucial with type 2 diabetes because too many carbs can increase blood glucose levels, which can damage blood vessels and lead to vision problems, kidney problems, and nerve problems.
Ariel Warren is a Registered Dietitian, Diabetes Educator, graduate from Brigham Young, and was diagnosed with Type 1 at the age of 4 years old. Ariel understands diabetes and enjoys working with clients to improve their blood sugar management, healthy eating, weight loss, fitness, and pregnancy. For coaching from a T1D Dietitian, you can contact Ariel directly, through her website: arielwarren.com.