The Role of Growth Hormone and Prolactin in Beta Cell Growth and Regeneration

Although the natural history of Type I diabetes mellitus does not support a significant regenerative capacity of the pancreatic beta cell there is, however, evidence for a substantial postnatal enlargement of the beta cell mass in both rodent and man.1,2 It was noted that the normal linear correlation between the logarithm of the body weight and the logarithm of the organ weight does not hold for the endocrine pancreas.3 As shown schematically in Figure I, the increase in the beta cell mass in the young rats lags behind that of the body weight, but catches up later in life. This may mean that the metabolic pressure on the beta cells during the rapid growth phase is not fully compensated for by a corresponding increase in the number of beta cells, which may explain the particular vulnerability of this cell type in childhood. During pregnancy there is a marked increase in the beta cell mass, which may reflect the increased demand for insulin during the considerable weight gain in the last trimester. In non-diabetic, obese humans, the islet mass is significantly greater than the islet mass of lean persons and that of obese patients with Type II diabetes.4 Thus the striking coincidence of diabetes of either type with periods of accelerated growth of the body as summarized in Table 1, may lead to speculations of a connection between the beta cell number and the susceptibility to develop diabetes. Because the growth hormone family, including prolactin and placental lactogen, are involved in many growth processes this review focuses on the possible role of these hormones in the growth and regeneration of the endocrine pancreas.5,6