Partially correct. Please allow me to explain. It is mentioned above: "shifting the equilibrium to the production of additional lactate, leading to hyperglycemia..."
It's true that excess NADH production as a result of alcohol consumption inhibits oxidation of lactate to pyruvate via lactate dehydrogenase. But, this leads to HYPOglycemia, not HYPERglycemia, because lactate is not adequately converted to pyruvate to meet the body's metabolic demands.
What are the repercussions?
Less pyruvate created ---> less of its conversion to oxaloacetate, which under normal conditions, would usually traverse across the mitochondrial membrane into the cytoplasm to be converted to PEP via PEPCK. Less oxaloacetate as a result of less pyruvate being shunted towards the gluconeogenesis pathway ultimately leads to HYPOglycemia.
Although ethanol on its own (like if you were to drink grain alcohol) would result in a drop in blood sugar, and this is ESPECIALLY a danger for individuals with Type 1 diabetes. Beer, wine, and common spirits rarely cause a drop in blood sugar because they also provide carbohydrates. These carbohydrates help to maintain blood sugar, if not elevate it on a binge.