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The influences of single-gene missense mutations expressing diabetes (db/db), obese (ob/ob) or dystrophia (dy/dy) dysregulated metabolic syndromes on hind limb bone maturation and cytodevelopment in C57BL/KsJ mice were evaluated by radiological, macro- and cytomorphometric analysis of the resulting variances in os coxae, femur and tibia osteodevelopment indices relative to control parameters between 8 and 16 weeks of age. Associated with obesity and hyperglycaemic/hyperinsulinaemic states, both db/db and ob/ob mutants demonstrated significant suppression of hind limb maturation (length) and cytodensity indices relative to control growth parameters. By contrast, skeletal growth suppression induced by dy/dy mutation expression was associated with lean body mass and normoglycaemic/hypoinsulinaemic systemic endometabolic indices. In both db/db and ob/ob mutation syndromes, osteovascular, -interstitial and -cytolipidaemia were prominent cytochemical aberrations of the osteopaenic states relative to the dyslipidaemia/fibrodysplasia characteristic of dy/dy osteomaturation. Between 8 and 16 weeks of age, both ob/ob and db/db groups demonstrated extensive cortical interstitial (laminal) osteolipidaemia and suppressed cytodensities compared to control indices. These data demonstrate that the abnormal hyperglycaemic/hyperinsulinaemic endometabolic states associated with the expression of db/db and ob/ob genomutations promote extensive lipidaemia-induced osteopaenia, compromising hind limb osteomaturation and cytodensity indices, as compared to the hyperfibritic osteopaenia characteristic of dy/dy mutation syndromes. Recognized therapeutic modulation of the hypercytolipidaemic component of diabetes-obesity syndromes may prove to be effective towards amelioration of the deleterious influences of these expressed hyperglycaemic, dysregulated lipometabolic conditions on osteomaturation and cytodevelopment.
Garris et al. (Tue,) studied this question.