In vivo and in vitro experiments have shown that nicotinamide enhances the regeneration of rat B cells. Nicotinamide has been administered to human subjects at a dose of 3 g/day for more than one year without any serious side effects. A trial was conducted to study if nicotinamide could protect B cells in Type I (insulin-dependent) diabetic patients with established diabetes, but still with residual insulin secretion, the latter being evaluated throughout the study period. A randomized double-blind study was carried out on 26 Type I diabetic patients aged 15 to 40 years who had been treated with insulin for 1 to 5 years but who had a residual insulin secretion characterized by a glucagon stimulated C-peptide level higher than 0.1 nmol/l. They were given either 3 g/day of nicotinamide or a placebo for nine months. At baseline the treated and control groups did not differ according to age, diabetes duration, insulin dose, HbA1c or C-peptide levels. Three patients dropped out of the study. At 9 months there were no significant changes in the insulin doses required. However, HbA1c rose in the control group (8.1 +/- 0.4 vs 9.8 +/- 0.5%, p less than 0.05) but not in the nicotinamide treated group (7.5 +/- 0.5 vs 6.9 +/- 0.4%).(ABSTRACT TRUNCATED AT 250 WORDS)

La asociación entre la obesidad y la densidad mineral ósea ha sido un punto controversial al momento de establecer si existe una asociación positiva o negativa entre las mismas. Diversos estudios han propuesto que la obesidad es un factor protector del hueso, debido a la tensión mecánica dada por el peso corporal en la remodelación ósea. Otros estudios plantean que la relación es mucho más compleja debido a que el tejido adiposo y los osteoblastos provienen de líneas germinales comunes. Además, el adipocito tiene la capacidad de secretar diversas moléculas, entre ellas las adipocinas. Adicionalmente, el tejido adiposo es una de las principales fuentes de aromatasa, esto lo involucra en la conversión de andrógenos a estrógenos, que juegan un papel importante en el mantenimiento de la homeostasis ósea. Por lo tanto, se ha planteado el hueso como órgano blanco de diversas vías endocrinas y, a su vez, se considera un órgano endocrino que puede afectar otros órganos cuando está alterado. Por otra parte, se ha visto que la resistencia a la insulina en el contexto de la obesidad está asociada con inflamación crónica de bajo grado, deterioro funcional de órganos y alteración del metabolismo energético, que impacta la remodelación ósea.   Abstract There is controversy over the effect of obesity in bone mineral density. Several studies have proposed that obesity is a protective factor of the bone by the mechanical tension that favors the bone remodeling. However, other studies suggest that this relationship is more complex because both tissues come from a common germ line; emphasizing that the adipocyte secretes diverse molecules, among them adipocinas. In addition, adipose tissue has aromatases that convert androgens into estrogens, having an importance in bone homeostasis. Therefore, the bone has been raised as a target organ of various endocrine pathways, which may affect other organs when it is altered. On the other hand, it has been shown that insulin resistance in the context of obesity is associated with chronic low-grade inflammation, functional impairment of organs and impaired energy metabolism, which impacts bone remodeling.

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