The Course of Development of Glucose Intolerance
in the Monkey (Macaco mulatta)

Cl, Hamilton; Ciaccia, PJ

doi:10.1159/000459806

Cited by 33 publications

(12 citation statements)

References 9 publications

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“…Sequential changes for monkeys with NIDDM, excluding those with abnormalities due to an islet lesion or pregnancy, have been noted by other investigators [Hamilton & Ciaccia, 1978;Hansen & Bodkin, 19851 and have been further corroborated in our studies. Hyperinsulinemia or other insulin abnormalities, whether fasting or secretory, can be apparent before there is overt carbohydrate intolerance; many of the hyperinsulinemic monkeys were normoglycemic and had normal carbohydrate clearance.…”

Section: Discussionsupporting

confidence: 90%

Carbohydrate impairment and insulin secretory abnormalities among Macaca mulatta from Cayo Santiago

Howard

Kessler

Schwartz

1986

American J Primatol

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macaques (Macaca mulatta) from Cay0 Santiago were examined for evidence of carbohydrate intolerance indicative of potential development of non-insulin-dependent diabetes mellitus (NIDDM). Monkeys 6 to > 20 years from natal Groups J, M, and P, an AGED Group (all >20 years), and unrelated monkeys removed from the island in association with other groups (CAYO), were examined with intravenous glucose tolerance tests (iv-GTT). Morphometric measurements were made on all tested monkeys. Impairments included fasting hyperglycemia ( > 115 mg/dl), impaired glucose clearance (K < 2.0%/min), fasting hyperinsulinemia (> 150 pU/ml) or hypoinsulinemia (< 20 pU/ml), and insulin secretory abnormalities (> 500 pU/ ml or < 75 pU/ml). Natal groups J and M had 31% with impairments, group P had 0% the AGED group had 45%, and the CAYO group had 33%. Impaired glucose clearance was usually attributable to a reduced insulin response. Impairments correlated significantly (p < 0.05) to body weight and a modified Quetelet index, but not to sex, acute stress, or islet cell antibodies; the relationships to age could not be delineated in this survey. Impairments in monkeys are indicative of various stages in the asynchronous development of carbohydrate intolerance leading to NIDDM.

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Section: Discussionsupporting

confidence: 90%

Carbohydrate impairment and insulin secretory abnormalities among Macaca mulatta from Cayo Santiago

Howard

Kessler

Schwartz

1986

American J Primatol

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“…As has been observed for humans, the overwhelming majority of cases reported in primates represent T2D and are associated with both obesity and increasing age (Wagner et al , 2001. These clinical observations that are similar to the human condition have been noted for rhesus and cynomolgus monkeys and for baboons (Banks et al 2003, Cai et al 2004Hamilton and Ciaccia 1978;Hotta et al 2001;Wagner et al 1996;Stokes 1986). The most remarkable similarity may be in the identification of the prediabetic phase, with the observation of insulin resistance and compensatory hyperinsulinemia as is well documented for the human condition (see Figure 1).…”

Section: Primate Modelsmentioning

confidence: 60%

Animal Models of Type 2 Diabetes: Clinical Presentation and Pathophysiological Relevance to the Human Condition

2006

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The prevalence of diabetes throughout the world has increased dramatically over the recent past, and the trend will continue for the foreseeable future. One of the major concerns associated with diabetes relates to the development of micro- and macrovascular complications, which contribute greatly to the morbidity and mortality associated with the disease. Progression of the disease from prediabetic state to overt diabetes and the development of complications occur over many years. Assessment of interventions designed to delay or prevent disease progression or complications in humans also takes years and requires tremendous resources. To better study both the pathogenesis and potential therapeutic agents, appropriate animal models of type 2 diabetes (T2D) mellitus are needed. However, for an animal model to have relevance to the study of diabetes, either the characteristics of the animal model should mirror the pathophysiology and natural history of diabetes or the model should develop complications of diabetes with an etiology similar to that of the human condition. There appears to be no single animal model that encompasses all of these characteristics, but there are many that provide very similar characteristics in one or more aspects of T2D in humans. Use of the appropriate animal model based on these similarities can provide much needed data on pathophysiological mechanisms operative in human T2D.

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“…As in humans, most NHPs with diabetes have T2DM (Wagner et al 1996b(Wagner et al , 2001. Similar to humans, T2DM is associated with increasing age and body weight in rhesus (Hamilton and Ciaccia 1978;Hotta et al 2001), in cynomolgus monkeys (Wagner et al 1996b), and in baboons (Banks et al 2003;Cai et al 2004;Stokes 1986). The disease initially is associated with normal glucose tolerance and insulin resistance with compensatory hyperinsulinemia, followed by continued deterioration of carbohydrate metabolism ( Figure 1) (Hansen and Bodkin 1986).…”

Section: Overview Of Diabetes In Old World Nhpsmentioning

confidence: 98%

Old World Nonhuman Primate Models of Type 2 Diabetes Mellitus

Wagner

Kavanagh²,

Ward³

et al. 2006

ILAR Journal

159

153

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Type 2 diabetes mellitus is a major health problem of increasing incidence. To better study the pathogenesis and potential therapeutic agents for this disease, appropriate animal models are needed. Old World nonhuman primates (NHPs) are a useful animal model of type 2 diabetes; like humans, the disease is most common in older, obese animals. Before developing overt diabetes, NHPs have a period of obesity-associated insulin resistance that is initially met with compensatory insulin secretion. When either a relative or absolute deficiency in pancreatic insulin production occurs, fasting glucose concentrations begin to increase and diabetic signs become apparent. Pathological changes in pancreatic islets are also similar to those seen in human diabetics. Initially there is hyperplasia of the islets with abundant insulin production typically followed by replacement of islets with islet-associated amyloid. Diabetic NHPs have detrimental changes in plasma lipid and lipoprotein concentrations, lipoprotein composition, and glycation, which may contribute to progression of atherosclerosis. As both the prediabetic condition (similar to metabolic syndrome in humans) and overt diabetes become better defined in monkeys, their use in pharmacological studies is increasing. Likely due to their genetic similarity to humans and the similar characteristics of the disease in NHPs, NHPs have been used to study recently developed agonists of the peroxisome proliferators-activated receptors. Importantly, agonists of the different receptor subclasses elicit similar responses in both humans and NHPs. Thus, Old World NHPs are a valuable animal model of type 2 diabetes to study disease progression, associated risk factors, and potential new treatments.

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The Course of Development of Glucose Intolerance in the Monkey (Macaco mulatta)

Cited by 33 publications

References 9 publications

Carbohydrate impairment and insulin secretory abnormalities among Macaca mulatta from Cayo Santiago

Carbohydrate impairment and insulin secretory abnormalities among Macaca mulatta from Cayo Santiago

Animal Models of Type 2 Diabetes: Clinical Presentation and Pathophysiological Relevance to the Human Condition

Old World Nonhuman Primate Models of Type 2 Diabetes Mellitus

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