As the explanation states, a low carb diet results in triacylglyceride (fatty acid (FA)) breakdown in adipose tissues for energy, since sugars are not being consumed. Yep, in the liver, the acetyl CoA will feed into krebs for a little bit and generate energy, but then once the adipose tissues start breaking down their FAs and sending the resulting glycerol and acetyl CoA to the liver, the acetyl CoA will inhibit PDH and activate pyruvate carboxylase. This will stimulate gluconeogenesis which, yes, will at first create oxaloacetate (OAA), but that OAA will quickly be turned into PEP and shunted up through the gluconeogenesis pathway to turn into exportable glucose (in the liver). The acetyl CoA (sent from the adipose tissue) which had previously inhibited PDH and stimulated pyruvate carboxylase will then be turned into ketone bodies in the liver, and sent as another exportable form of energy (for the brain, and other tissues that use ketone bodies).
SOOOOO moral of the story, the ketone bodies will INCREASE in the blood levels on a low carb diet, but the OAA will be turned into PEP (IN the liver cells, NOT the blood) to increase glucose concentrations in the blood stream.