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Experimental diabetes because of STZ or other models associated with insulin deficiency results in gastric and colonic dilatation and loose stools. Schmidt et al. (20) described distal axonal swellings and dystrophic changes in the ileal mesentery of diabetic rats, containing a variety of normal and unusual subcellular organelles similar to those described in experimental and clinical axonal dystrophies. These alterations, consisting a distinctive distal axonopathy involving terminal axons and synapses, are particularly dense in the prevertebral superior mesenteric ganglia and celiac ganglia. These axonal alterations were seen after 6, 9, and 12 months of diabetes, apparently increasing in frequency with time. The changes were not seen at 3.5 months. An apparent proximo-distal gradient in the frequency of unmyelinated axonal lesions in this system, suggests experimental DAN may represent an example of distal axonopathy. Retrograde axonal transport of nerve growth factor was reduced (21). Aldose reduction inhibition was reported to partially reduce the development of these dystrophic changes (22). In a recent study, these workers reported that the changes were more prominent in the STZ-D rat and BB/Wor rat, both models of hypoinsulinemic type 1 diabetes, than in the BBZDR/Wor rat, a hyperglycemic and hyperinsulinemic type 2 diabetes model. They argued that hyperglycemia alone is not sufficient to produce sympathetic ganglionic neuroaxonal dystrophy, but rather that it may be the diabetes-induced superimposed loss of trophic support that ultimately causes these lesions (23). Similar findings to the pancreas have been reported (24). In a study of diabetes induced by STZ and occurring spontaneously in BB/W rats, morphometric analysis of contacts between [3H]norepinephrine-labeled sympathetic nerve terminals and a-cells in pancreases from STZ-D rats revealed a 65-70% reduction in direct contacts. An 80% reduction in the number of nerve endings in direct contact with a-cells was also noted in the BB/W diabetic rats.

These structural changes tend to be well-developed only in very chronic diabetes, typically studies done on rats that had been diabetic for 1 year or more. For instance, in a study of diabetes because of STZ, for a duration of 1 year, florid pathological changes were found on light and electronmicroscopy (25). The changes included changes in sympathetic neurons, with intra-axonal glycogen deposits, accumulation of large amounts of lipoid material in autonomic ganglion cells and endoneural cells. By morphometry, the cytoplas-mic area and cytoplasmic to nuclear ratio were significantly reduced in the sympathetic neurons of diabetic rats. The axons demonstrated dwindling in the sympathetic pregan-glionic fibers of diabetic animals. Axonal glycogenosomes were absent in the vagus of control and were present in that of diabetic rats.

In a wide survey of sympathetic adrenergic innervation of nerves, adrenergic nerves were studied in nervi nervorum and perivascular nerve plexus of vasa nervorum in whole-mount nerve sheath preparations of optic, sciatic, and vagus nerves and in the paravertebral sympathetic chain in normal and STZ-treated diabetic rats. A substantial or complete loss of fluorescent adrenergic fibres around blood vessels in the optic nerves was observed 8 weeks after induction of diabetes; whereas perivascular adrener-gic fibres in the sciatic, vagus, and sympathetic chain nerve trunks were increased at that early time-point.

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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