B12 is too large a molecule to be absorbed in the colon's membrane - it has evolved to be absorbed in the ileum, a segment at the end of the small intestine, and requires an intrinsic factor mediated system. Other apes either need to eat their own feces - coprophagy -  to absorb B12 or eat animal products (insects or small prey). Nutritional requirements for other apes are not well known but B12 deficiency is a well known problem in humans. 

The ileum is the major site of absorption of vitamin B12 analogues

Abstract

Non-cobalamin vitamin B12 analogues constitute a significant percentage of total corrinoids in human serum. The source and means of absorption of analogues and their significance are largely unknown. We studied the sites of production and absorption of B12 analogues by measuring serum vitamin B12 and analogues in 93 patients with various gastrointestinal diseases: pernicious anemia (PA), ileal resections, ileitis, Crohn's colitis, ulcerative colitis, and irritable bowel syndrome (IBS). Patients with PA had normal analogue levels that were unchanged or that rose during cessation of B12 administration. Patients with IBS, Crohn's colitis, ulcerative colitis, and total colectomies had B12 analogues in the normal range. Patients with diseased or resected ileums had low B12 and analogues. These data suggest that serum B12 analogues are absorbed in the ileum by a mechanism independent of intrinsic factor, and that colonic bacteria and endogenous metabolism of vitamin B12 do not contribute significantly to their level.

Vitamin B12 deficiency

Abstract

Vitamin B12 (cobalamin) deficiency is a common cause of macrocytic anemia and has been implicated in a spectrum of neuropsychiatric disorders. The role of B12 deficiency in hyperhomocysteinemia and the promotion of atherosclerosis is only now being explored. Diagnosis of vitamin B12 deficiency is typically based on measurement of serum vitamin B12 levels; however, about 50 percent of patients with subclinical disease have normal B12 levels. A more sensitive method of screening for vitamin B12 deficiency is measurement of serum methylmalonic acid and homocysteine levels, which are increased early in vitamin B12 deficiency. Use of the Schilling test for detection of pernicious anemia has been supplanted for the most part by serologic testing for parietal cell and intrinsic factor antibodies. Contrary to prevailing medical practice, studies show that supplementation with oral vitamin B12 is a safe and effective treatment for the B12 deficiency state. Even when intrinsic factor is not present to aid in the absorption of vitamin B12 (pernicious anemia) or in other diseases that affect the usual absorption sites in the terminal ileum, oral therapy remains effective.

Vitamin B12 synthesis by human small intestinal bacteria

Abstract

In man, physiological amounts of vitamin B12 (cyanocobalamin) are absorbed by the intrinsic factor mediated mechanism exclusively in the ileum. Human faeces contain appreciable quantities of vitamin B12 or vitamin B12-like material presumably produced by bacteria in the colon, but this is unavailable to the non-coprophagic individual. However, the human small intestine also often harbours a considerable microflora and this is even more extensive in apparently healthy southern Indian subjects. We now show that at least two groups of organisms in the small bowel, Pseudomonas and Klebsiella sp., may synthesise significant amounts of the vitamin.