Most mammals synthesise ascorbic acid in the liver from glucose. The final step requires L-gulonolactone oxidase, and in guinea pigs the gene encoding it is a non-functional pseudogene. Humans, other haplorrhine primates and some bats carry independent losses of the same gene, so the trait arose separately rather than by shared inheritance.
The consequence is dietary. A guinea pig deprived of vitamin C develops scurvy within weeks: impaired collagen synthesis, joint pain, poor wound healing and haemorrhage. Requirements are usually cited around 10 to 30 milligrams per kilogram per day, higher for pregnant animals, and are met with fresh vegetables or supplemented pellets, since ascorbic acid degrades in stored feed.
That vulnerability made the species historically important. Guinea pigs were central to early twentieth-century work identifying vitamin C and to the demonstration that scurvy is a deficiency disease. The phrase guinea pig for an experimental subject dates from about the same period, though today most laboratory work uses mice and rats instead.