Observations on Offspring of Mice Made Diabetic With Streptozocin

Abstract

My objective was to determine the effect of streptozocin (STZ)-induced diabetes in male inbred mice on nonfasting blood glucose levels and body weights of offspring. Hyperglycemia was induced in CBA/H male mice by either multiple subdiabetogenic doses (MD) of STZ (5 doses/day of 50 mg STZ/kg body wt) or by a single high sublethal (SD) dose (200 mg STZ/kg body wt). Females were made diabetic by the multiple low-dose procedure. The following matings were set up: SD males with normal (NOR) females; MD males with NOR females; NOR males with MD females; MD males with MD females. Controls were matings of NOR males with NOR females. Among the first cohort of litters was born one female from the cross of an SD male with an NOR female who became spontaneously hyperglycemic at 5 wk of age; the female progeny of this cross had significantly lower body weights. All other progeny groups were normoglycemic (up to 5 wk) and had normal body weights. Test progeny weaned in the second and subsequent cohorts of litters were also normoglycemic. The major effect in this progeny group was on body weight; diabetic fathers (particularly MD males) mated with NOR females produced offspring with significantly higher juvenile body weights than the controls (increase of approximately 0.5 g). These body-weight distributions also appeared more homogeneous than the more variable body-weight distribution of the controls. In contrast, MD mothers (mated with NOR males) produced second-cohort offspring with significantly lower average body weights (decrease of approximately 1-2 g) than the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin‐related peptides and the two‐cell block to development in pre‐implantation mouse embryos

“…Reports of in vivo insulin supplementation in maternal diabetic rats assisting the early growth (from one-cell stage) of the pre-implantation embryo may be a result of an improved maternal 'metabolic environment' and are not due to any direct insulin effects upon the early embryo (Steele 1988, Beebe & Kaye 1990. As glucose in high concentrations has also been shown to be toxic to early embryos (Zusman et al 1985, De Hertogh et al 1991, in vivo addition of insulin may cause glucose depletion in oviductal and uterine fluids and reduce embryonic toxicity.…”