Spontaneous Diabetes in Macaca Nigra

Howard, Charles F.

doi:10.2337/diab.21.11.1077

Cited by 50 publications

(27 citation statements)

References 10 publications

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“…Spontaneous diabetes mellitus or carbohydrate mismanagement occurs commonly among monkeys [9][10][11], There are fewer reports of diabetes in prosimians. To our knowledge, there is only one reference to diabetes in apes, namely the one reported by Reut her [17] of a diabetic male chimpan zee in the San Francisco Zoo.…”

Section: Introductionmentioning

confidence: 99%

Diabetes mellitus in the Chimpanzee (Pan troglodytes)

Iy¹,

Ta²,

Cf³

1981

J Med Primatol

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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.

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Section: Introductionmentioning

confidence: 99%

Diabetes mellitus in the Chimpanzee (Pan troglodytes)

Iy¹,

Ta²,

Cf³

1981

J Med Primatol

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“…A high incidence of spontaneous diabetes mellitus has been found in Macaca nigra (Celebes black apes) [1]. Although diabetes has been diagnosed in occasional members of several non-human primate species [2--7], more than 50% of the Macaca nigra present diabetic signs of apparently increasing frequency and severity.…”

Section: Introductionmentioning

confidence: 99%

Diabetes in Macaca nigra: Metabolic and histologic changes

Howard

1974

Diabetologia

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Summary. Expanded studies on the spontaneous diabetes mellitus in Macaca nigra provide additional support to analogies between this animal mode] and human diabetes. Abnormal signs include hyperglycemia, decreased clearance of glucose in intravenous tolerance tests, reduced insulin secretion and increased serum lipids (triglyceride, prebetalipoprotein and nonesterified fatty acids). Insulin secretory capacity is lost concomitant with amyloid infiltration into the islets of Langerhans; additional metabolic aberrations may also reduce insulin secretion or action. Secondary manifestations are atherosclerosis, thickened basement membranes of muscle capillaries, and cataracts. In all probability, a genetic predisposition in these monkeys is exacerbated by changes in diet and environment.

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“…39,42 Other animal models of spontaneous autoimmune diabetes include the LEW.1AR1/ Ztm-iddm rats, 43 the Keeshond dog, 44 and the Celebes black ape (Macaca nigra). 45 In addition to these main animal models of T1D, genetically and virally induced models are available for research purposes. The AKITA mouse was derived in Akita, Japan, from a C57BL/6NSlc mouse with a spontaneous mutation in the insulin 2 gene, which results in a severe insulindependent diabetes beginning at 3-4 weeks of age, and is used to study the success of islet transplantation.…”

mentioning

confidence: 99%

Diabetes reversal via gene transfer: building on successes in animal models

Gerace¹,

Martiniello‐Wilks²,

Simpson³

2015

RRED

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Type 1 diabetes (T1D) is caused by the autoimmune destruction of the insulinproducing pancreatic β-cells. People with T1D manage their hyperglycemia using daily insulin injections; however, this does not prevent the development of long-term diabetic complications such as retinopathy, nephropathy, neuropathy, and various macrovascular disorders. Currently, the only "cure" for T1D is pancreas transplantation or islet-cell transplantation; however, this is hampered by the limited number of donors and the requirement for life-long immunosuppression. As a result, the need for alternative therapies is vital. One of the strategies employed to correct T1D is the use of gene transfer to generate the production of an "artificial" β-cell that is capable of secreting insulin in response to fluctuating glucose concentrations that normally occurs in people without T1D. The treatment of many diseases using cell and gene therapy is generating significant attention in the T1D research community; however, for a cell therapy to enter clinical trials, success and safety must first be shown in an appropriate animal model. Animal models have been used in diabetes research for over a century, have improved our understanding of the pathophysiology of diabetes, and have led to the discovery of useful drugs for the treatment of the disease. Currently, the nonobese diabetic mouse is the animal model of choice for the study of T1D as it most closely reflects disease development in humans. The aim of this review is to evaluate the success of cell and gene therapy to reverse T1D in animal models for future clinical application.

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Spontaneous Diabetes in Macaca Nigra

Cited by 50 publications

References 10 publications

Diabetes mellitus in the Chimpanzee (Pan troglodytes)

Diabetes mellitus in the Chimpanzee (Pan troglodytes)

Diabetes in Macaca nigra: Metabolic and histologic changes

Diabetes reversal via gene transfer: building on successes in animal models

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