Acetyl-CoA can be metabolized through the TCA in any cell, but it can also undergo a different process in liver cells: ketogenesis, which produces ketone bodies.[27] Ketone bodies are also produced in mitochondria, and usually occur in response to low blood glucose levels.[28] When glucose levels are low, oxaloacetate is diverted away from the TCA cycle and is instead used to produce glucose de novo (gluconeogenesis). But when oxaloacetate is unavailable to condense with acetyl-CoA, acetyl-CoA cannot enter the cycle, and so the body has evolved an alternative way to harvest energy from it.
It is known that different dietary components exert some effects on gut microbiome composition, mainly in relation to obesity and inflammatory states. In general, a Mediterranean diet has a positive effect while a high-protein diet seems to have detrimental effects due to putrefaction phenomena (Lopez-Legarrea et al., 2014; Flint et al., 2015). Few data are available at this time about the effects of KD on gut microbiota. For example, a study by Crawford et al. (2009) investigated the regulation of myocardial ketone body metabolism by the gut microbiota and demonstrated that, during fasting, the presence of gut microbiota improved the supply of ketone bodies to the heart where KBs were oxidized. In the absence of a microbiota, low levels of KB was associated with a related increase in glucose utilization, but heart weight was still significantly reduced. The myocardial-mass reduction was completely reversed in germ-free mice feeded with a ketogenic diet. Regarding food control we can hypothesize that the particular metabolic state of ketosis could provide some benefit to weight and food control via synergic actions between butyrate production by gut bacteria and circulating high blood ketones (Sanz et al., 2015).
The second type of cellular fuel comes from fat and fat metabolism products called ketone bodies.   The average sized human body can store hundreds of thousands of calories in the form of fat, so we could say that this system of energy is almost unlimited, depending on how long one goes without food.  Eventually, it would get used up, but people have been known to fast for months and live through it.

The discovery of many appetite-related hormones provided molecular basis for appetite control, decreasing the relevance of the metabolites hypothesis (Karatsoreos et al., 2013). Recently, Sumithran et al. demonstrated that there is a long-term persistence of changes in some peripheral hormones involved in food control (Sumithran et al., 2011). In this study, they found a significant difference in mean levels of many food intake-related hormones 1 year after the cessation of weight loss via the hypocaloric diet. There was a long lasting decrease of anorexigenic compounds: leptin, PYY, cholecystokinin, insulin, and pancreatic peptide and an increase of the orexigenic molecule ghrelin. Moreover, they found that hunger remained elevated 1 year after diet cessation. In a successive study the same group investigated hunger-related hormones after 8 weeks of KD, demonstrating that during ketosis the increase of ghrelin (a strong stimulator of appetite) was suppressed (Sumithran et al., 2013). These results are consistent with those of Ratliff et al (Ratliff et al., 2009), who found no significant change in fasting plasma ghrelin after 12 weeks of VLCD.

Net carbs is simply total carbs minus fiber and non-digestible sugar alcohols, like erythritol. (This doesn’t apply to high glycemic sugar alcohols, like maltitol.) We don’t have to count fiber and certain sugar alcohols in net carbs, because they either don’t get broken down by our bodies, are not absorbed, or are absorbed but not metabolized. (Read more about sugar alcohols here.)
Jump up ^ Ringberg TM, White RG, Holleman DF, Luick JR (1981). "Body growth and carcass composition of lean reindeer (Rangifer tarandus tarandusL.) from birth to sexual maturity" (PDF). Canadian Journal of Zoology. 59 (6): 1040–1044. doi:10.1139/z81-145. ISSN 0008-4301. Body growth and carcass composition were measured in lean reindeer during the juvenile growth period between birth and 3 years of age. Mean carcass weight in these lean reindeer was 56 ± 4% of body weight and the deposition of body muscle and bone mass was linearly correlated with body weight after the 1st month of age. The weight of the brain relative to body weight and carcass weight declined, while the relative changes in heart, liver, kidneys, parotid glands, and tissues of the gastrointestinal tract were small after the neonatal period. The extractable fat content in carcasses increased from 4.4 to 11.4% of wet weight or approximately 100 g fat at birth and 3.5 kg fat in adult reindeer. Fat-free dry matter represented a constant percentage (18–20%) of wet carcass weight independent of body weight after the neonatal period, while a significant inverse relationship between carcass fat and body water was found.
There are three instances where there’s research to back up a ketogenic diet, including to help control type 2 diabetes, as part of epilepsy treatment, or for weight loss, says Mattinson. “In terms of diabetes, there is some promising research showing that the ketogenic diet may improve glycemic control. It may cause a reduction in A1C — a key test for diabetes that measures a person’s average blood sugar control over two to three months — something that may help you reduce medication use,” she says.
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