Islet recovery and reversal of murine type 1 diabetes in the absence of any infused spleen cell contribution

A cure for type 1 diabetes will probably require the provision or elicitation of new pancreatic islet beta cells as well as the reestablishment of immunological tolerance. A 2003 study reported achievement of both advances in the NOD mouse model by coupling injection of Freund's complete adjuvant with infusion of allogeneic spleen cells. It was concluded that the adjuvant eliminated anti-islet autoimmunity and the donor splenocytes differentiated into insulin-producing (presumably beta) cells, culminating in islet regeneration. Here, we provide data indicating that the recovered islets were all of host origin, reflecting that the diabetic NOD mice actually retain substantial beta cell mass, which can be rejuvenated/regenerated to reverse disease upon adjuvant-dependent dampening of autoimmunity.     

Effects of different supplemental sugars and starch fed in combination with degradable intake protein on low-quality forage use by beef steers.

Twenty ruminally fistulated steers (Exp. 1, 448 kg and Exp. 2, 450 kg) were used in two consecutive randomized complete block experiments with five treatments in each experiment. The purpose was to evaluate the impact of feeding different supplemental sugars or starch in combination with supplemental degradable intake protein (DIP) on the utilization of low-quality tallgrass-prairie hay. In Exp. 1, steers were given ad libitum access to forage and, except for the negative control (NC), received a limited supply (insufficient to maximize forage use) of supplemental DIP (.031% BW/d, DM basis). In addition to the NC, this experiment included four supplementation treatments in which one of four carbohydrate (CHO) sources (starch, glucose, fructose, or sucrose) was fed at .30% BW of DM/d. In Exp. 2, the treatment structure was identical except that the supplemental DIP level (.122% BW, DM basis) was near the level needed to maximize forage use. Forage OM intake (FOMI) was not affected (P> or =.26) by supplementation in Exp. 1 but was increased (P = .05) in Exp. 2. However, no difference (P> or =.46) in FOMI occurred among CHO sources in either experiment. Total OM and digestible OM intakes were increased (P<.01) by supplementation in both experiments. In Exp. 1, no difference (P>.26) in OM digestion (OMD) occurred among treatments. In Exp. 2, supplementation increased (P<.01) OMD. Additionally, sugars yielded a higher (P = .04) OMD than starch, and the monosaccharides yielded a higher (P = .02) OMD than sucrose. In Exp. 1, NDF digestion (NDFD) was decreased (P = .02) by supplementation, but no differences (P> or =.21) occurred among CHO sources. In Exp. 2, NDFD was increased (P = .03) by supplementation. Additionally, sugars led to higher (P = .05) NDFD than starch, and the monosaccharides led to higher (P = .03) NDFD than sucrose. In both experiments, discernible patterns were observable with regard to the effects of supplementation and type of supplemental CHO on ruminal fermentation characteristics. In conclusion, even though some consistency in fermentation profiles for different carbohydrate sources was evident in both experiments, forage intake and digestion responses were not consistent across experiments. This raises the possibility that carbohydrate source may interact with the amount of supplemental DIP fed and, as such, deserves additional investigation.