Diabetes mellitus in the Chimpanzee (Pan troglodytes)

Abstract

Glucose intolerance was found in four adult chimpanzees. The response of glucose, insulin, C-peptide, and glucagon to intravenous glucose and tolbutamide stimulations revealed impaired glucose clearance, deficient pancreatic secretion of insulin and C-peptide, and elevated glucagon levels. Pancreatic islets in a diabetic chimpanzee were hypercellular, possibly due to α-cells. Minimal or no insulin was observed in β-cells. Results are consistent with the occurrence of noninsulin-dependent diabetes mellitus, which may be more prevalent in chimpanzees than heretofore suspected.

Spontaneous Diabetes Mellitus in Animals

“…Spontaneous diabetes mellitus in humanoid and non-humanoid primates was described in captive animals and it is consistent with clinical and morphological features of type 2 diabetes mellitus [133][134][135][136][137][138][139]. Thus, previous results, comparative studies and creation of animal models emphasized many similarities with human non-insulin dependent diabetes mellitus (insulin resistance, long prediabetic status and impaired -cell function).…”

Control of Insulin mRNA Stability in Rat Pancreatic Islets

“…Had it been possible to perform experimental studies with chimpanzee islets, it would have been very interesting to determine whether insulin mRNA levels in the chimpanzee are governed by the same signals as in rodent and human islets. Type 2 diabetes mellitus has been observed in the chimpanzee and may be more frequent than expected (31).…”

Nonhuman Primates and other Animal Models in Diabetes Research

“…49 Chimpanzees (Pan troglyodytes) also develop spontaneous diabetes. 51,52 Categorically, these NHPs all exhibit clinical features of diabetes, including obesity, IR, dyslipidemia, and pancreatic pathology that are similar to those observed in humans 37,49,53 and are therefore excellent models for studying human T2DM. In many NHPs, T2DM is associated with increased age and body weight 37,39,41,42,[54][55][56][57] and is initially characterized by normal glucose tolerance that is followed by IR, a compensatory increase in insulin secretion, and deterioration of carbohydrate metabolism.…”