Naturally occurring left ventricular hyperplasia is a rare but lethal disease. There are very few reports of this cardiac disease in captive nonhuman primates. In a colony of Macaca mulatta (Rhesus monkey) at California National Primate Research Center, a large number of rhesus macaques were diagnosed by autopsy with naturally occurring left ventricular hypertrophy without obvious underlying diseases over a 22-year period. The confirmatory diagnosis of ventricular hypertrophy was based on findings of notable left ventricular concentric hypertrophy with reduced left ventricular lumen, which is very similar to human ventricular hypertrophy cases. This report discusses an 11-year-old Macaca fascicularis monkey (Cynomolgus monkey, crab-eating macaque), weighing 2.95 kg, that was presented for enrollment in a pharmacokinetic (PK) study. During the PK experiment, the monkey died following a sudden decrease in percutaneous oxygen saturation and heart rate. Gross and histological examinations of the heart were performed. On gross pathology, the left ventricular wall was thickened, and the chamber lumen was reduced. In histopathological examination using hematoxylin- eosin and Masson-trichrome stains, fibrosis and myocyte disarray were not observed, but an increased cell density, compared to the normal heart, was confirmed. The autopsy results confirmed left ventricular hyperplasia as the major cause of death.

Many biological systems are regulated by an intricate set of feedback loops that oscillate with a circadian rhythm of roughly 24 h. This circadian clock mediates an increase in body temperature, heart rate, blood pressure, and cortisol secretion early in the day. Recent studies have shown changes in the amplitude of the circadian clock in the hearts and livers of streptozotocin (STZ)-treated rats. It is therefore important to examine the relationships between circadian clock genes and growth factors and their effects on diabetic phenomena in animal models as well as in human patients. In this study, we sought to determine whether diurnal variation in organ development and the regulation of metabolism, including growth and development during the juvenile period in rats, exists as a mechanism for anticipating and responding to the environment. Also, we examined the relationship between changes in growth factor expression in the liver and clock-controlled protein synthesis and turnover, which are important in cellular growth. Specifically, we assessed the expression patterns of several clock genes, including Per1, Per2, Clock, Bmal1, Cry1 and Cry2 and growth factors such as insulin-like growth factor (IGF)-1 and -2 and transforming growth factor (TGF)-β1 in rats with STZ-induced diabetes. Growth factor and clock gene expression in the liver at 1 week post-induction was clearly increased compared to the level in control rats. In contrast, the expression patterns of the genes were similar to those observed after 5 weeks in the STZ-treated rats. The increase in gene expression is likely a compensatory change in response to the obstruction of insulin function during the initial phase of induction. However, as the period of induction was extended, the expression of the compensatory genes decreased to the control level. This is likely the result of decreased insulin secretion due to the destruction of beta cells in the pancreas by STZ.