Ketone body：Ketone bodies, or simply ketones are substances produced by the liver during gluconeogenesis, a process which creates glucose in times of fasting and starvation. There are three ketone bodies produced by the liver. They are acetoacetate, D-beta-hydroxybutyrate (D-BHB), and acetone. These compounds are used in healthy individuals to provide energy to the cells of the body when glucose is low or absent in the diet.

Ketone bodies , D-β-hydroxybutyrate (D-BHB) support mammalian survival during states of energy deficit by serving as alternative source of ATP. D-BHB levels are elevated during starvation, high-intensity exercise or by the low carbohydrate ketogenic diet. Prolonged caloric restriction or fasting reduces inflammation as immune system adapts to low glucose supply and energy metabolism switches towards mitochondrial fatty acid oxidation, ketogenesis and ketolysis.

Ketone body provides aternative fuel to glucose：When your body relies on glucose as its primary fuel, you’re also relying heavily on the proper function of the hormone insulin. Insulin acts as a chauffeur to shuttle glucose into your cells so it can be used for fuel.The problem is, acute infection (bacterial and viral) can invoke insulin resistance. That means that when you’re fighting off these infections, your ability to utilize glucose is impaired.Insulin resistance is associated with a wide range of metabolic imbalances such as enhanced oxidative stress, inflammation, high blood triglycerides, low HDL cholesterol, high LDL cholesterol, and an increased risk for diabetes and heart disease.Unless your cells have another source of fuel, you may not get the proper nourishment your body needs to get well — and you could also be driving further imbalances.Fortunately, when you follow a keto diet, you provide your cells with an alternative fuel source that can take over for glucose, and doesn’t require insulin as a chauffeur into energy-hungry cells.Ketone body blocks the NLRP3 inflammasome-mediated inflammatory diseaseD-Beta hydroxybutyrate reduced the NLRP3 inflammasome mediated IL-1β and IL-18 production in human monocytes. In vivo, BHB attenuates caspase-1 activation and IL-1β secretion in mouse models of NLRP3-mediated diseases like Muckle-Wells Syndrome (MWS), Familial Cold Autoinflammatory syndrome (FCAS) and urate crystal induce body cavity inflammation. Taken together, these findings suggest that the anti-inflammatory effects of caloric restriction or ketogenic diets may be mechanistically linked to BHB-mediated inhibition of the NLRP3 inflammasome, and point to the potential use of interventions that elevate circulating D-Beta hydroxybutyrate against NLRP3-mediated proinflammatory diseases. These findings provide insight into immunological functions of metabolic signals such as D-Beta hydroxybutyrate and suggest that dietary or pharmacological approaches to elevate D-BHB, without inducing the generalized starvation response, holds promise in reducing the severity of multiple NLRP3 mediated chronic inflammatory diseases.