Abnormal insulin secretion and glucose metabolism in pancreatic islets from the spontaneously diabetic GK rat

Östenson, Claes‐Göran; Khan, Abdul Waheed; Abdel‐Halim, Samy M.; Guenifi, Amel; Suzuki, Ken; Gotō, Yoshio; Efendić, Suad

doi:10.1007/bf00399086

Cited by 230 publications

(208 citation statements)

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“…Other studies using GK rats originating from local colonies have also documented an impaired insulin secretory response [7,8]. Nevertheless it was claimed that such impairment in the London colony was not related to a reduced pancreatic insulin content [8], whereas decreased as well as normal pancreatic insulin content, together with normal islet beta-cell density, have been reported in adult GK rats in the Stockholm colony [7,9,10]. These conflicting data led us to document more extensively the beta-cell mass in GK rats originating from the Paris colony.…”

Section: Discussionmentioning

confidence: 92%

“…Plasma insulin release in vivo in response to intravenous glucose was lacking and in vitro studies of insulin release with isolated perfused pancreas or perifused islets [6] indicated that both early and late phases of glucose-induced insulin release were markedly affected in the adult GK rat. Other studies using GK rats originating from local colonies have also documented an impaired insulin secretory response [7,8]. Nevertheless it was claimed that such impairment in the London colony was not related to a reduced pancreatic insulin content [8], whereas decreased as well as normal pancreatic insulin content, together with normal islet beta-cell density, have been reported in adult GK rats in the Stockholm colony [7,9,10].…”

Section: Discussionmentioning

confidence: 99%

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Impaired development of pancreatic beta-cell mass is a primary event during the progression to diabetes in the GK rat

et al. 1997

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Established non-insulin-dependent diabetes mellitus (NIDDM) is associated with profound insulin secretory defects that occur together with insulin resistance. The basis for the insulin secretory defects is unknown and is difficult to study in human subjects because it is not possible to identify prospectively those subjects in whom glucose control will deteriorate. The fact that total beta-cell mass is decreased in NIDDM patients compared to weight-matched control subjects [1] offers strong support for the notion that insulin production may become insufficient if beta-cell growth is deficient. The contribution of decreased beta-cell mass to deficient insulin secretion Diabetologia (1997) 40: 916-925 Impaired development of pancreatic beta-cell mass is a primary event during the progression to diabetes in the GK rat

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Impaired development of pancreatic beta-cell mass is a primary event during the progression to diabetes in the GK rat

et al. 1997

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Section: Discussionmentioning

confidence: 99%

“…Several animal models for NIDDM have been described. Although recent studies have revealed impaired insulin secretion in GK rats [5][6][7], most of the animal models for NIDDM are characterized by obesity, hyperinsulinaemia and islet hypertrophy [8].The NSY (Nagoya-Shibata-Yasuda) mouse is a spontaneous model of NIDDM with moderate obesity that was established by selective breeding for glucose intolerance from a non-diabetic JcI:ICR mouse colony [9]. Previous studies suggested that NSY mice develop renal lesions similar to diabetic nephro-…”

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confidence: 99%

The NSY mouse: a new animal model of spontaneous NIDDM with moderate obesity

et al. 1995

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SummaryThe NSY (Nagoya-Shibata-Yasuda) mouse was established as an inbred strain of mouse with spontaneous development of diabetes mellitus, by selective breeding for glucose intolerance from outbred Jcl:ICR mice. NSY mice spontaneously develop diabetes mellitus in an age-dependent manner. The cumulative incidence of diabetes is 98 % in males and 31% in females at 48 weeks of age. Neither severe obesity nor extreme hyperinsulinaemia is observed at any age in these mice. Glucose-stimulated insulin secretion was markedly impaired in NSY mice after 24 weeks of age. In contrast, fasting plasma insulin level was higher in male NSY mice than that in male C3H/He mice (545 +73 vs 350+ 40 pmol/1, p < 0.05, at 36 weeks of age). Pancreatic insulin content was higher in male NSY mice than that in male C3H/He mice (76 + 8 vs 52 _+ 5 ng/mg wet weight, p < 0.05, at 36 weeks of age). Morphologically, no abnormal findings, such as hypertrophy or inflammatory changes in the pancreatic islets, were observed in NSY mice at any age. These data suggest that functional changes of insulin secretion in response to glucose from pancreatic beta cells may contribute to the development of non-insulin-dependent diabetes mellitus (NIDDM) in the NSY mouse. Although insulin sensitivity was not measured, fasting hyperinsulinaemia in NSY mice suggests that insulin resistance may also contribute to the pathogenesis of NIDDM. Since these findings are similar to the pathophysiologic features of human NIDDM patients, the NSY mouse is considered to be useful for investigating the pathogenesis and genetic predisposition to NIDDM. [Diabetologia (1995) 38: 503-508] Key words NSY mouse, non-insulin-dependent diabetes mellitus, animal model, insulin secretion, isolated islets.Non-insulin-dependent diabetes mellitus (NIDDM) is a heterogeneous disorder, caused by an interaction of genetic and environmental factors [1][2][3]. This heterogeneity in human NIDDM makes it difficult to clarify the genetics or pathogenesis of the disease. Animal models are invaluable for the analysis of heterogeneous disorders such as diabetes. This is eviReceived: 22 June 1994 and in revised form: 11 October 1994 Corresponding author: Dr. H. Ikegami, Department of Geriatric Medicine, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan Abbreviations: NIDDM, Non-insulin-dependent diabetes mellitus; IDDM, insulin-dependent diabetes mellitus; NSY mouse, Nagoya-Shibata-Yasuda mouse.denced by the recent progress in the understanding of the genetics and pathogenesis of insulin-dependent diabetes mellitus by use of excellent animal models, such as the nonobese diabetic (NOD) mouse and the Bio-Breeding (BB) rat [4]. Several animal models for NIDDM have been described. Although recent studies have revealed impaired insulin secretion in GK rats [5][6][7], most of the animal models for NIDDM are characterized by obesity, hyperinsulinaemia and islet hypertrophy [8].The NSY (Nagoya-Shibata-Yasuda) mouse is a spontaneous model of NIDDM with moderate obesity that was establ...

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“…GK rats exhibit moderate but enhanced fasting glucose levels, evident from 6 weeks of age, due to decreased beta cell secretion of insulin (Ostenson et al 1993). Also, GK rats present normal lipidemia, peripheral and hepatic insulin resistance, and late complications, such as nephropathy or neuropathy.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Bioenergetics, Diabetes, and Aging: Top-Down Analysis Using the Diabetic Goto-Kakizaki (GK) Rat as a Model

Ferreira¹,

Moreno²,

Seiça³

et al. 2006

Toxicology Mechanisms and Methods

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Abnormal insulin secretion and glucose metabolism in pancreatic islets from the spontaneously diabetic GK rat

Cited by 230 publications

References 24 publications

Impaired development of pancreatic beta-cell mass is a primary event during the progression to diabetes in the GK rat

Impaired development of pancreatic beta-cell mass is a primary event during the progression to diabetes in the GK rat

The NSY mouse: a new animal model of spontaneous NIDDM with moderate obesity

Mitochondrial Bioenergetics, Diabetes, and Aging: Top-Down Analysis Using the Diabetic Goto-Kakizaki (GK) Rat as a Model

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