By what mechanism can hypoglycemia induce fainting?
There are regulatory mechanisms that may prevent moderate hypoglycemia to progress to a more severe state, however these mechanisms act before lack of conciousness sets in. The progression of hypoglycemia may depend on overall health and medical status and vary between healthy and diabetic persons, for example.

Rosenthal et al. (1) write that


  The brain is normally dependent on glucose for oxidative metabolism
  and function. Acute iatrogenic hypoglycemia, occurring as a result of
  insulin excess during the treatment of type 1 diabetes, can cause
  clinically significant cognitive impairment. In health, such
  hypoglycemic cognitive dysfunction does not occur. Endogenous
  counterregulatory mechanisms are activated in response to a small
  reduction in circulating glucose, preventing more profound
  hypoglycemia. In diabetes, the inability to reduce circulating insulin
  levels (1), the failure of glucagon responses (2), sometimes
  accompanied by defective autonomic and adrenergic responses (3), can
  allow plasma glucose levels to fall low enough to result in detectable
  disturbance of cognitive function, ranging from a subtle slowing of
  reaction times (3) to coma (4).


In short, the brain malfunctions due to lack of glucose (the sole energy source for the brain). Note that cognitive impairment and unconciousness can also occur in otherwise healthy persons, for example in the case of prolonged exercise combined with lack of nutrition. The exact cause of cortical dysfunction is not known:


  Impairment of brain function is a recognized consequence of acute
  hypoglycemia. It is known that different brain functions have
  different susceptibilities to acute hypoglycemia; for example, the
  triggering of autonomic activation, a hypothalamic function, occurs in
  response to quite modest decrements in circulating glucose
  concentrations (5,6,7), whereas significant cortical dysfunction
  requires more profound glucose deprivation (3). Even within different
  cortical functions, there is variation in hypoglycemia susceptibility
  (26). The mechanisms of cortical dysfunction during hypoglycemia are
  not known.