This is the study I posted earlier on MS and type 1 diabetes, but I think it is worth repeating. The researchers concluded that patients with type 1 diabetes are at an enormously increased risk of multiple sclerosis. The researchers found a 20-fold increase in the prevalence of MS in type 1 diabetic women. There must be some pretty strong common links between these two diseases.
Type 1 diabetes and multiple sclerosis: together at last.
Dorman JS, Steenkiste AR, Burke JP, Songini M. 2003. Diabetes Care 10.2337/diacare.26.11.3192 vol. 26 no. 11 3192-3193
“examination of data collected for our Familial Autoimmune and Diabetes (FAD) Study revealed, for the first time, a highly significantly increased prevalence of multiple sclerosis in adults with type 1 diabetes and their first-degree relatives…Thus, we observed a 20-fold increase in the prevalence of multiple sclerosis in our type 1 diabetic women…We therefore conclude that adult women with type 1 diabetes are at an enormously increased risk of multiple sclerosis, and that the answer to questions about the clustering of these disorders is that they are together at last.”
Acetylcholine would be one factor joining these two diseases together and our old friend "homocysteine" would be another. Researchers in the following study stated that "as homocysteine exerts detrimental effects on endothelial and neuronal cells, this study investigated effects of acute homocysteine exposure on beta-cell function and insulin secretion." ...
J Endocrinol. 2006 May;189(2):301-10.
Detrimental actions of metabolic syndrome risk factor, homocysteine, on pancreatic beta-cell glucose metabolism and insulin secretion.
Patterson S, Flatt PR, Brennan L, Newsholme P, McClenaghan NH.
Elevated plasma homocysteine has been reported in individuals with diseases of the metabolic syndrome including vascular disease and insulin resistance. As homocysteine exerts detrimental effects on endothelial and neuronal cells, this study investigated effects of acute homocysteine exposure on beta-cell function and insulin secretion using clonal BRIN-BD11 beta-cells. Acute insulin release studies in the presence of various test reagents were performed using monolayers of BRIN-BD11 cells and samples assayed by insulin radioimmunoassay. Cellular glucose metabolism was assessed by nuclear magnetic resonance (NMR) analysis following 60-min exposure of BRIN-BD11 cell monolayers to glucose in either the absence or presence of homocysteine. Homocysteine dose-dependently inhibited insulin release at moderate and stimulatory glucose concentrations. This inhibitory effect was reversible at all but the highest concentration of homocysteine. 13C-glucose NMR demonstrated decreased labelling of glutamate from glucose at positions C2, C3 and C4, indicating that the tricarboxylic acid (TCA) cycle-dependent glucose metabolism was reduced in the presence of homocysteine. Homocysteine also dose-dependently inhibited insulinotropic responses to a range of glucose-dependent secretagogues including nutrients (alanine, arginine, 2-ketoisocaproate), hormones (glucagon-like peptide-1 (7-36)amide, gastric inhibitory polypeptide and cholecystokinin-8), neurotransmitter (carbachol), drug (tolbutamide) as well as a depolarising concentration of KCl or elevated Ca2+. Insulin secretion induced by activation of adenylate cyclase and protein kinase C pathways with forskolin and phorbol 12-myristate 13-acetate were also inhibited by homocysteine. These effects were not associated with any adverse action on cellular insulin content or cell viability, and there was no increase in apoptosis/necrosis following exposure to homocysteine. These data indicate that homocysteine impairs insulin secretion through alterations in beta-cell glucose metabolism and generation of key stimulus-secretion coupling factors. The participation of homocysteine in possible beta-cell demise merits further investigation.
In the following study the researchers link the peripheral neuropathy found in patients with diabetes with impaired exocrine pancreatic function. The researchers stated that compared to normal controls, all diabetics exhibited a significant reduction in both enzyme and bicarbonate secretion to all stimuli.
Impaired exocrine pancreatic function in diabetics with diarrhea and peripheral neuropathy.El Newihi, H., C.P. Dooley, C. Saad, J. Staples, A. Zeidler, J.E. Valenzuela. 1998. Dig Dis Sci. 33(6):705-10.
“…Compared to normals, all diabetics exhibited a significant reduction in both enzyme and bicarbonate secretion to all stimuli. This reduction was not corrected by administering bethanechol…We conclude that diabetics with diarrhea and peripheral neuropathy exhibit impairment of their exocrine pancreatic secretion…”
In the next study the researchers stated their results show that exocrine pancreatic function is impaired in a high percentage of both type 1 and type 2 diabetics. The researchers concluded that diabetes secondary to pancreatic exocrine disease could be much more frequent than believed so far.
Pancreatic exocrine function in patients with type 1 and type 2 diabetes mellitus.
Hardt, P.D., A. Krauss, L. Bretz, M. Porsch-Özcürümez, H. Schnell-Kretschmer, E. Mäser, R.G. Bretzel, T. Zekorn, L. Bretz, H.U. Klör. 2000. Acta Diabetologica Volume 37, Issue 3, pp 105-110.
“Reduced exocrine pancreatic function has been observed in a high percentage of patients with type 1 diabetes in the past…In this study we investigated exocrine pancreatic function in 105 controls and 114 with type 1 or type 2 diabetes mellitus by means of an indirect test (faecal elastase-1 concentration). This test has good sensitivity and specificity for moderate and severe pancreatic insufficiency as compared to the gold standard. Reduced faecal elastase-1 concentrations were found in 56.7% of type 1 patients, 35% of type 2 patients and 18.1% of the controls…The data found for type 1 patients correspond to those reported in earlier studies. The results for type 2 diabetics show that exocrine pancreatic function is also impaired in a high percentage in this group of patients…Observations from autopsies and the data of the controls in this study suggest that chronic pancreatitis might be a common problem. In consequence, diabetes secondary to exocrine disease could be much more frequent than believed so far.”
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