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This overview gives a brief historical summary of key discoveries regarding stem cells of the small intestine. The current concept is that there are two pools of intestinal stem cells (ISCs): an actively cycling pool that is marked by Lgr5, is relatively homogeneous and is responsible for daily turnover of the epithelium; and a slowly cycling or quiescent pool that functions as reserve ISCs. The latter pool appears to be quite heterogeneous and may include partially differentiated epithelial lineages that can reacquire stem cell characteristics following injury to the intestine. Markers and methods of isolation for active and quiescent ISC populations are described as well as the numerous important advances that have been made in approaches to the in vitro culture of ISCs and crypts. Factors regulating ISC biology are briefly summarized and both known and unknown aspects of the ISC niche are discussed. Although most of our current knowledge regarding ISC physiology and pathophysiology has come from studies with mice, recent work with human tissue highlights the potential translational applications arising from this field of research. Many of these topics are further elaborated in the following articles. [ABSTRACT FROM AUTHOR]

The Bar Harbor obese-hyperglycemic mouse (ob/ob) characteristically develops its obese phenotype during the postweaning period, when access to food is unrestricted and its behavioral phenotype of hyperphagia appears. In the present study suckling behavior (viz., nipple attachment latencies and total suckling time) of lean and preobese mouse pups, derived from matings of heterozygous lean parents, was measured in either fed or fasted conditions from 6 to 21 days postpartum on anesthetized dams. Twenty-hour milk deprivation selectively channeled pup activity into suckling for both preobese and lean mice, although, in general, preobese mice nipple-attached sooner and suckled longer than leans. In particular, fed preobese pups suckled longer than fed lean pups from 18 days on, providing a preweaning behavioral indicant of a genetic tendency to obesity when environmental constraints on overeating are minimized. [ABSTRACT FROM AUTHOR]