This report provides information on the morphology of fat absorption in rat intestinal epithelial cells. Three types of experiments were performed: (a) intubation of corn oil into fasted rats, (b) injection of physiological fatty-chyme prepared from fat-fed donor rats into ligated segments of jejunum of fasted animals, and (c) administration of electron-opaque particles in corn oil and markers given concurrently with the fat. These results support the hypothesis that fat is absorbed by selective diffusion of monoglycerides and fatty acids from micelles rather than by pinocytosis of unhydrolized triglycerides. Evidence is presented that the pits between the microvilli, previously believed to function in the transport of fat, are not involved in this process. Instead they appear to contribute their contents to lysosomes in the apical cytoplasm. Arguments are offered that the monoglycerides and fatty acids diffuse from the micelle while the latter is associated with the microvillous membrane of the absorptive cell. These micellar components penetrate the plasma membrane and diffuse into the cytoplasmic matrix where they encounter the SER. Triglyceride synthesis occurs in the SER and results in the deposition of fat droplets within its lumina. The synthesis of triglycerides and their sequestration into the SER establishes an inward diffusion gradient of monoglycerides and fatty acids.

Hydrostatic pressure, when applied to segments of the small intestine of the salamander, causes a tremendous reduction in number of microvilli and a loss of the terminal web . The intestinal epithelium strips off from its deeper layers at the level of the basement membrane . When the pressure is released and this epithelial sheet is allowed to recover, the microvilli and its terminal web reappear . Stages in the reformation of microvilli are described . In the earliest stages, foci of dense material seem to associate with the cytoplasmic surface of the apical plasma membrane . From this material, filaments appear and their regrowth is correlated with the extension of the microvilli . We suggest that the dense material nucleates the assembly of the filaments which, in turn, appear instrumental in the redevelopment of microvilli . This concept is supported by the existing literature . Further, since neither the microvilli nor the terminal web reappear on any surface but the apical surface, even though the apical and basal surfaces are bathed with the same medium, we suggest that information in the membrane itself or directly associated with the membrane dictates the distribution of the dense material which leads to the formation of the microvilli and ultimately to the polarity of the cell . 408

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Hepatic glycogen patterns are described for rats adapted to a precisely controlled feeding schedule and ad libitum fed rats. Liver samples were processed for biochemical and histochemical glycogen analysis at precise intervals following a 22 hour fast and a 2 hour meal. Histochemical determination of glycogen (PAS) after freeze substitution showed lobular patterns of hepatic glycogen which correlate with chemically determined glycogen levels and nutritional states of the rats. After 22 hour fasting, hepatocytes from rats with low glycogen levels (< 0.09% ) exhibited no significant staining. In control fed rats, feeding caused glycogen deposition throughout the lobule but in greatest concentration centrilobularly throughout the early phases of glycogen accumulation. As glycogen deposition continued, periportal lobular patterns were observed in rats with high glycogen levels (> 5% ). Glycogen depletion reduced glycogen staining in cells throughout the lobule, but centrilobular patterns prevailed until late in depletion when periportal patterns appeared. Ad libitum-fed rats showed similar glycogen patterns except maximum deposition was characterized by centrilobular or even lobular distribution of glycogen, and periportal patterns of glycogen were seen only rarely in extreme fasted rats. Differences in lobular patterns between ad libitum and control fed rats is apparently related to lower maximum hepatic glycogen levels reached by ad libitum-fed animals.The mammalian liver is important in regulating blood glucose by storing and breaking down hepatic glycogen after appropriate stimulation. Many biochemical details of glycogenolysis and glycogenesis have been reported and much work has been directed toward elucidating the control mechanisms of these processes. (Scrutton and Utter, '68; Robison et al., '68; Villar-Palasi and Larner, '70; Ryman and Whelan, '71). A problem of considerable importance for studies of glycogen metabolism at the cellular level is an accurate description of glycogen patterns in the liver during deposition and depletion of the carbohydrate.In general, investigators have agreed that hepatic intralobular differences in glycogen distribution exist during a cycle of feeding and fasting, but the precise pattern was unclear. Bock and Hoffman (1872) reported that liver glycogen in rabbits was deposited initially around the central vein and only later in more peripheral regions. This finding was confirmed in studies of livers from a variety of species AM. J. ANAT., 140: 299-338.by several workers (Noel, '23; Kater, '33; Forsgren, '35; Eger and Ottensmeir, '52; Themann, '63; Corrin and Aterman, '68). In contrast to this, others claimed that glycogen deposition proceeded from the periphery of the lobule to more centrally situated hepatocytes (Smith, '31; Kater, '33; Edlund and Holmgren, '40; Deane, '44; Ekman and Holmgren, '49).Literature on glycogen patterns during depletion also presents conflicting results. Noel ('23) reported that hepatic glycogen patterns during glycogenolysis were the reve...