Viruses and the Pathogenesis of Diabetes Mellitus

Rayfield, Elliot J.; Seto, Yoshiko

doi:10.2337/diab.27.11.1126

Cited by 90 publications

(29 citation statements)

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“…Furthermore, the DNA content of 50 control and infected islets was virtually identical (data not shown). (1)(2)(3)(4)(5)35). In the case of infection with both Coxsackie B4 virus and the M variant of EMC virus in genetically susceptible mice, an acute diabeteslike syndrome develops within 7 d. The severity of hyperglycemia correlates closely pathologically with the degree of pancreatic damage (4).…”

Section: Methodsmentioning

confidence: 99%

Virus-induced alterations in insulin release in hamster islets of Langerhans.

Rayfield¹,

Seto²,

Walsh³

et al. 1981

J. Clin. Invest.

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A B S T R A C T After the inoculation of Golden Syrian hamsters with the TC-83 vaccine strain of Venezuelan encephalitis (VE) virus, a sustained diminution in glucose-stimulated insulin release and glucose intolerance of shorter duration develops. To understand better the mechanism of this defect in insulin release, we examined insulin secretion in response to several test agents in isolated perifused islets from control and 24-d post-VE virus-infected hamsters. 50 islets were used in all perifusion experiments, and data were expressed as total insulin released as well as peak response for each test agent during a 30-min perifusion period from control and VE-infected islets. After perifusion with 20 mM glucose, a 45% diminution of insulin release was noted in VE-infected islets in comparison with control islets, which in turn was similar to in vivo findings. However, following 1-mM tolbutamide stimulation, insulin release was similar in control and VE-infected islets. In separate studies, 1 mM tolbutamide, 10 mM theophilline, 1 mM dibutyryl cyclic (c)AMP, and 1 mM 8-bromo-cAMP resulted in statistically similar insulin-release curves in control and VE-infected islets. Additional experiments assessing [5_3H]glucose use in control and infected islets after 20 min ofperifusion with 20 mM glucose revealed virtually identical values (239±30-control; and 222 ±27-VE-infected islets). Morphological and morphometric evaluation of VE-infected islets (21 d following virus inoculation) showed no changes in islet volume density, beta cell density, and beta cell granulation. Thus, VE virus induces a defect in glucose-stimulated insulin release from hamster beta cells that can be corrected by cAMP analogues and does not alter islet glucose use.

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Section: Methodsmentioning

confidence: 99%

Virus-induced alterations in insulin release in hamster islets of Langerhans.

Rayfield¹,

Seto²,

Walsh³

et al. 1981

J. Clin. Invest.

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“…In previous studies no association between these virus infections and the onset of Type 1 diabetes was found [5][6][7]. Although mumps infection may result in transient ICA, islet cell surface antibodies and insulin-autoantibody responses [t9 -20], and may occasionally cause Type i diabetes [21], there is little evidence that these viruses are a significant cause of Type 1 diabetes.…”

Section: Discussionmentioning

confidence: 99%

No association between islet cell antibodies and coxsackie B, mumps, rubella and cytomegalovirus antibodies in non-diabetic individuals aged 7?19 years

et al. 1991

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Summary. Viral antibodies were tested in a cohort of 44 isletcell antibody-positive individuals age 7-19 years, and 44 of their islet cell antibody-negative age and sex-matched classmates selected from a population study of 4208 pupils who had been screened for islet cell antibodies. Anti-coxsackie B1-5 IgM responses were detected in 14 of 44 (32 %) of the islet cell antibody-positive subjects and in 7 of 44 (16 % ) control subjects. This difference did not reach the level of statistical significance. None of the islet cell antibody-positive subjects had specific IgM antibodies to mumps, rubella, or cytomegalovirus. There was also no increase in the prevalence or the mean titres of anti-mumps-IgG or IgA and anti-cytomegalovirus-IgG in islet cell antibody-positive subjects compared to control subjects. These results do not suggest any association between islet cell antibodies, and possibly insulitis, with recent mumps, rubella or cytomegalovirus infection. Further studies are required to clarify the relationship between islet cell antibodies and coxsackie B virus infections.

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“…according to their report, FT1DM accounts for around 20% of the ketosisonset type 1 diabetes cases in Japan and has more se-in FT1DM [3,5,21]. More studies including the pancreas histology will be needed to clarify whether patients with abrupt onset autoimmune type 1 diabetes also exhibit nonspecific inflammation to the exocrine pancreas as well as the specific insulitis.…”

Section: Discussionmentioning

confidence: 99%

A Case of Abrupt Onset Autoimmune Type 1 Diabetes Mimicking Fulminant Type 1 Diabetes

et al. 2009

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Abstract.A 63-year-old male was admitted to our hospital with diabetic ketoacidosis. He had flu-like symptoms 10 days before admission and developed thirst, polyuria and anorexia with 9 kg of body weight loss in a week. Plasma glucose level on admission was 983 mg/dL and hba1c was 7.5%. Despite high levels of serum pancreatic enzymes, lack of severe abdominal pain and no morphological change of pancreas in the abdominal CT scan eliminated the complication of classical acute pancreatitis. These findings suggested the diagnosis of fulminant type 1 diabetes. However, urinary and plasma C-peptide levels showed that insulin secretion was not completely depleted at onset. Furthermore, an examination of isletrelated antibodies revealed the presence of high titer anti-GaD antibody. his hLa typing showed that DRb1*0901-DQb1*0303 and a24 were present. he has been doing well with continuation of insulin therapy. Over two years after onset, his plasma C-peptide level was gradually lowered, and anti-GaD antibody was still positive. Taken together, this is a rare case of abrupt onset autoimmune type 1 diabetes with transient but apparent exocrine pancreatic impairment at onset. Similar cases should be accumulated to clarify pathophysiological similarities and/or differences between fulminant type 1 diabetes and abrupt onset autoimmune type 1 diabetes. (FT1DM) is a novel clinical entity which is characterized by an extremely abrupt onset of the disease and remarkably acute destruction of pancreatic beta cells with urinary C-peptide secretion less than 10 µg/day: however, more than 90% of FT1DM patients were adolescent or adult [3][4][5]. although FT1DM is basically classified into type 1B diabetes as indicated by absence of islet-related autoantibodies, two atypical cases showing the mixed characteristics of FT1DM and autoimmune type 1 diabetes (i.e. anti-GaD antibody positivity) have been reported [6,7]. here we report a 63-year-old case of abrupt onset autoimmune type 1 diabetes, mimicking FT1DM. in addition to the above mentioned two autoimmune cases [6,7], the present case draws an attention in terms of differential diagnosis between typical FT1DM and this rapidly progressive form of autoimmune type 1 diabetes. Case Reporta 63-year-old male was admitted to our hospital with diabetic ketoacidosis on December 23 in 2006. his medical history revealed that he had been suffering from hypertension and angina pectoris for 7 years, but there was no sign of diabetes. The hba1c level in June, 2006 was 5.5%, while fasting plasma glu-

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Viruses and the Pathogenesis of Diabetes Mellitus

Cited by 90 publications

References 0 publications

Virus-induced alterations in insulin release in hamster islets of Langerhans.

Virus-induced alterations in insulin release in hamster islets of Langerhans.

No association between islet cell antibodies and coxsackie B, mumps, rubella and cytomegalovirus antibodies in non-diabetic individuals aged 7?19 years

A Case of Abrupt Onset Autoimmune Type 1 Diabetes Mimicking Fulminant Type 1 Diabetes

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