Pancreatic β-cell function in tropical pancreatic diabetes

Mohan, Viswanathan; Snehalatha, Chamukuttan; Ramachandran, Ambady; Jayashree, R.; Viswanathan, M

doi:10.1016/0026-0495(83)90053-7

Cited by 49 publications

(23 citation statements)

References 7 publications

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“…However, they are resistant to ketosis on withdrawal of insulin even for several weeks. (3) A history of cassava ingestion is very common.Recently, an explanation for the ketosis-resistant nature of tropical pancreatic diabetes has been put forward [7]. The present study demonstrates an interesting clinical and biochemical spectrum of tropical pancreatic diabetes as seen in the state of Tamitnadu (Madras) in South India.…”

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confidence: 73%

Tropical pancreatic diabetes in South India: heterogeneity in clinical and biochemical profile

et al. 1985

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Summary.Clinical and Nochemical studies were carried out in 33 patients with diabetes secondary to chronic calcific, nonalcoholic pancreatitis (tropical pancreatic diabetes) and in 35 Type 2 (non-insulin-dependent) diabetic patients and 35 nondiabetic subjects. Despite lower body mass indices, only 250./0 of patients with tropical pancreatic diabetes had clinical evidence of malnutrition. There was no history of cassava ingestion. Mean serum cholesterol concentration was significantly lower in the tropical pancreatic diabetic patients (p < 0.01) in comparison with the Type 2 diabetic patients or non-diabetic subjects, due to a significantly decreased concentration of LDL cholesterol (p < 0.01) and VLDL cholesterol (p < 0.05). Basal and post-glucose stimulated concentrations of serum Cpeptide were highest in those pancreatic diabetic patients (n = 11) who responded to oral hypoglycaemic drugs, intermediate in the majority (n = i7), who were insulin dependent and ketosis resistant and negligible in a small sub-group (n = 5) who were ketosis prone. The occurrence of microangiopathy in pancreatic diabetic patients was common and similar to that in Type 2 diabetic patients. Thus, tropical pancreatic diabetes in South India appears to be heterogenous with respect to level of nutrition, severity of glucose intolerance, B-cell function, response to therapy and the occurrence of microvascular complications.Key words: Tropical pancreatic diabetes, heterogeneity, keto= sis-resistant, C-peptide, microangiopathy.While classical Type I (insulin-dependent) diabetes and Type 2 (non-insulin-dependent) diabetes are two well characterized entities of the diabetic syndrome, there are certain types of diabetes which do not fit into either of these categories. In tropical countries, diabetes associated with malnutrition, such as J-type diabetes [1,2] and tropical pancreatic diabetes [3-6[, have been described. Earlier studies have suggested the following characteristics of tropical pancreatic diabetes [5,6]: (1) Patients belong to the lowest socio-economic strata of society and appear grossly emaciated with signs of severe protein-calorie malnutrition. (2) They have severe insulin-dependent diabetes and often require large doses of insulin for stabilization of the diabetes. However, they are resistant to ketosis on withdrawal of insulin even for several weeks. (3) A history of cassava ingestion is very common.Recently, an explanation for the ketosis-resistant nature of tropical pancreatic diabetes has been put forward [7]. The present study demonstrates an interesting clinical and biochemical spectrum of tropical pancreatic diabetes as seen in the state of Tamitnadu (Madras) in South India. Subjects and methodsSubjects studied were attending the M.V.Hospita[ for Diabetes, Madras, a large referral centre for diabetes in South India.The tollowing criteria were used for diagnosis of tropical pancreatic diabetes : (1) a history of recurrent abdominal pain fi'om an early age; (2) the presence of pancreatic calculi seen on plain abdominal ...

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confidence: 73%

Tropical pancreatic diabetes in South India: heterogeneity in clinical and biochemical profile

et al. 1985

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“…Partial preservation of beta cell function as shown by Cpeptide studies. [50][51][52][53] 2. Decreased glucagon reserve.…”

Section: Diabetesmentioning

confidence: 99%

Tropical Chronic Pancreatitis

Mohan

Premalatha

Pitchumoni

2003

Journal of Clinical Gastroenterology

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“…In contrast, FCPD (previously known as tropical pancreatic diabetes) can be well defined, e.g. diabetes associated with chronic pancreatitis not due to a known cause of pancreatitis (for instance, alcoholism, gall stones, etc); the patient usually requires insulin for control of hyperglycaemia and is still ketosis resistant, frequently has a low body mass index (less than 18), evidence of pancreatic calculi on plain abdominal x-ray and often a past history of recurrent abdominal pain in childhood [4][5][6][7].…”

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The genetic predisposition to fibrocalculous pancreatic diabetes

et al. 1989

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Summary. Fibrocalculous pancreatic diabetes (previously known as tropical pancreatic diabetes) is a rare cause of diabetes confined to countries within the tropical belt. The aetiology of fibrocalculous pancreatic diabetes is thought to be environmental although the agent(s) is unknown. We have investigated a possible genetic basis of this disease by looking for restriction fragment length polymorphisms of genes implicated in the aetiology of diabetes rnellitus. Seventy-six Dravidian patients with fibrocalculous pancreatic diabetes were studied, and the restriction fragment length polymorphisms obtained compared to racially matched control subjects (n=94), patients with Type2 (non-insulin-dependent) diabetes (n=87) and Type 1 (insulin-dependent) diabetes (n = 58). No association of fibrocalculous pancreatic diabetes was found with restriction fragment length polymorphisms of the insulin receptor gene. Although no association of fibrocalculous pancreatic diabetes was found with polymorphism of the HLA DRc~/DQc~/DXct genes, an association was found with the Taq 1 restriction fragment length polymorphisms of the DQ[~ gene (DQ[~ T2/T6 present in 39% of patients with fibrocalculous pancreatic diabetes compared to 19% in control subjects; p = 0.01 ; corrected p value = 0.04) which is similar to that found in Type 1 but not Type 2 diabetes. An association of fibrocalculous pancreatic diabetes was also found with the hypervariable region in the 5-prime flanking region of the insulin gene; 40% of patients possessed the class 3 allele compared to 9.5% of control subjects p = 0.0001 ; corrected p value = 0.0008). In Type 2 diabetes, similar results were obtained with 33% subjects possessing the class 3 allele (t7 value compared to control subjects = 0.0005; corrected p value = 0.004). This study suggests that fibrocalculous pancreatic diabetes has a genetic component in its aetiology. Furthermore, its origin might be related to an individual with part of the genetic predisposition to diabetes (Type 1 or Type 2) who additionally has evidence of chronic calcific pancreatitis.

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Pancreatic β-cell function in tropical pancreatic diabetes

Cited by 49 publications

References 7 publications

Tropical pancreatic diabetes in South India: heterogeneity in clinical and biochemical profile

Tropical pancreatic diabetes in South India: heterogeneity in clinical and biochemical profile

Tropical Chronic Pancreatitis

The genetic predisposition to fibrocalculous pancreatic diabetes

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