For over thirty years it has been known that enteroendocrine cells derive from common precursor cells in the intestinal crypts. Until recently relatively little was understood about the events that result in commitment to endocrine differentiation or the eventual segregation of over 10 different hormone expressing cell types in the gastrointestinal tract. Enteroendocrine cells arise from pluripotent intestinal stem cells. Differentiation of enteroendocrine cells is controlled by the sequential expression of three basic helix loop helix transcription factors, Math1, Neurogenin 3, and NeuroD. Math1 expression is required for specification and segregation of the intestinal secretory lineage (Paneth, goblet, and enteroendocrine cells) from the absorptive enterocyte lineage. Neurogenin 3 represents the earliest stage of enteroendocrine differentiation and in its absence enteroendocrine cells fail to develop. Subsequent expression of NeuroD appears to represent a later stage of differentiation for maturing enteroendocrine cells. Enteroendocrine cell fate is inhibited by the Notch signaling pathway, which appears to inhibit both Math1 and Neurogenin 3. Understanding enteroendocrine cell differentiation will become increasingly important for identifying potential future targets for common diseases like diabetes and obesity.
We investigated the differences in the Fourier transform infrared (FTIR) spectra of normal and abnormal human placentas. Normal placentas, placentas with infant intrauterine growth restriction (IUGR), and placentas from mothers with diabetes mellitus (DM) were used, none of which had been treated before measurement. The tissues were divided into three parts: the upper one‐third portion (P1), the middle portion (P2), and the lower one‐third portion (P3). Placental tissues were also investigated histochemically. The differences of the main second‐derivative FTIR spectra among P1, P2, and P3 in normal placentas were observed in bands appearing between 1080 and 1090 cm−1. Bands in P2 were observed at 1083 cm−1, which was significantly higher than that in P3 (p < 0.05). The spectrum of P2 tissue in placentas with infant IUGR had a peak at 1081 cm−1, which was significantly different from those of P1 and P3 (p < 0.05). In placentas with DM, the P2 band was shifted to a peak at 1088 cm−1. These data were well correlated with the histochemical sugar‐chain staining pattern of the P2 portion of the placenta. Our data suggested that this IR technique is applicable to the clinical diagnosis of diseases in the gynecological field. © 2000 John Wiley & Sons, Inc. Biopolymers (Biospectroscopy) 62: 22–28, 2001
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