PREVENTION AND REVERSAL DESPITE HYPERGLYCEMIA OF GLYCOGEN INFILTRATION (“HYDROPIC DEGENERATION”) IN THE PANCREAS IN ALLOXAN DIABETES IN THE RABBIT<sup>1</sup>

Duff, G. W.; Toreson, Wilfred E.

doi:10.1210/endo-48-3-298

Cited by 21 publications

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“…glucose administration in ob/ob mice 26 and after 8 h of glucose infusion in normal rats. 27 Glycogen also accumulates in diabetic states 28 and during treatment with corticosteroids. 29 Finally, glycogen deposition has also been associated with an enhanced response to theophylline.…”

Section: Discussionmentioning

confidence: 99%

Abnormalities of Insulin Responses After Ambient and Previous Exposure to Glucose in Streptozocin-diabetic and Dexamethasone-treated Rats: Role of Hyperglycemia and Increased B-Cell Demands

Grill

Rundfeldt

1986

Diabetes

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In NIDDM, B-cells are insensitive to glucose. We studied the specificity and evolution of this abnormality in 6-10-wk-old neonatally streptozocin-diabetic (STZ) and in dexamethasone-treated (DMT) rats. Not only the effect of ambient but also that of previous glucose (priming effect) was characterized in the perfused pancreas. In fed STZ, blood glucose was elevated to 9.2 +/- 0.8 versus 5.3 +/- 0.2 mM in control (C) rats. Ambient glucose (27 mM) in the perfusate induced a significant but reduced total response (11% of C) that was predominantly monophasic. Secretion was promptly induced (in less than 20 s) both in STZ and C. Other nutrients, i.e., glyceraldehyde (10 mM) and alpha-ketoisocaproic acid (KIC) (5 mM) also induced reduced and monophasic responses, whereas, in contrast, 3-isobutyl-1-methylxanthine (IBMX) induced an enhanced response that was 3.8-fold larger than in C. In DMT, blood glucose was normal (5.4 +/- 0.3 mM). Ambient glucose (27 mM) in the perfusate induced a normal first phase and a moderately reduced second phase (52% of untreated rats). DMT rats were hyperresponsive to IBMX, this agent inducing 2.5-fold higher release than in untreated rats. Previous perfusion with 27 mM glucose enhanced twofold the effect of a second stimulation period with glucose in C. This induction of priming by glucose could not be demonstrated in fed STZ or in DMT. However, when STZ were fasted or insulin treated for 36 h, induction of priming reappeared, i.e., the second pulse of glucose evoked 2-3-fold more insulin release than the first pulse.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Abnormalities of Insulin Responses After Ambient and Previous Exposure to Glucose in Streptozocin-diabetic and Dexamethasone-treated Rats: Role of Hyperglycemia and Increased B-Cell Demands

Grill

Rundfeldt

1986

Diabetes

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“…Professor Lyman Duff, whom we are proud to claim as a Toronto graduate in Medicine (he is now Dean of Medicine at McGill), has kindly sent me examples of what we used to call hydropic degeneration, but now know from the work of Toreson and Duff 14 to be glycogen infiltration. Similar conditions can be demonstrated in metapituitary diabetes in dogs where the glycogen is found in the degenerated islet and duct cells.…”

Section: The Source Of Insulinmentioning

confidence: 99%

Insulin: The Banting Memorial Lecture 1952

Best

1952

Diabetes

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Prevention and reversal of glycogen infiltration in the pancreatic islets of fetuses from diabetic rats

Kim

1965

Anat. Rec.

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Fetuses removed by Caesarean section (between days 17 and 21 of pregnancy) were compared with litter-mates removed at autopsy (between days 21 and 23).In one diabetic group, all rats were treated with a large dose of insulin until Caesarean section when insulin treatment was stopped. No fetuses removed by Caesarean section showed glycogen infiltration when blood sugar was less than 240 mg/100 ml. At autopsy, glycogen appeared in all fetuses from mothers which had blood sugar levels above 240 mg/100 ml for two days or longer; no glycogen appeared in fetuses from mothers which had blood sugar levels below 240 mg/100 ml.In another diabetic group, all rats were treated with insulin, but the insulin dose was increased immediately after Caesarean section. All fetuses removed by Caesarean section showed glycogen infiltration when the blood sugar level was greater than 240 mg/100 ml. At autopsy, glycogen had disappeared in fetuses from mothers which had blood sugar levels less than 240 mg/100 ml for 2 to 3 days; glycogen persisted in fetuses from mothers which had blood sugar levels above 240 mg/100 ml.It is concluded that glycogen appears in fetal islets if blood sugar level is greater than 240 mg/100 ml for two days or longer. This change is both preventable and reversible and is influenced by the level of blood sugar and by the duration of hyperglycemia.

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PREVENTION AND REVERSAL DESPITE HYPERGLYCEMIA OF GLYCOGEN INFILTRATION (“HYDROPIC DEGENERATION”) IN THE PANCREAS IN ALLOXAN DIABETES IN THE RABBIT¹

Cited by 21 publications

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Abnormalities of Insulin Responses After Ambient and Previous Exposure to Glucose in Streptozocin-diabetic and Dexamethasone-treated Rats: Role of Hyperglycemia and Increased B-Cell Demands

Abnormalities of Insulin Responses After Ambient and Previous Exposure to Glucose in Streptozocin-diabetic and Dexamethasone-treated Rats: Role of Hyperglycemia and Increased B-Cell Demands

Insulin: The Banting Memorial Lecture 1952

Prevention and reversal of glycogen infiltration in the pancreatic islets of fetuses from diabetic rats

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PREVENTION AND REVERSAL DESPITE HYPERGLYCEMIA OF GLYCOGEN INFILTRATION (“HYDROPIC DEGENERATION”) IN THE PANCREAS IN ALLOXAN DIABETES IN THE RABBIT1

Cited by 21 publications

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Abnormalities of Insulin Responses After Ambient and Previous Exposure to Glucose in Streptozocin-diabetic and Dexamethasone-treated Rats: Role of Hyperglycemia and Increased B-Cell Demands

Abnormalities of Insulin Responses After Ambient and Previous Exposure to Glucose in Streptozocin-diabetic and Dexamethasone-treated Rats: Role of Hyperglycemia and Increased B-Cell Demands

Insulin: The Banting Memorial Lecture 1952

Prevention and reversal of glycogen infiltration in the pancreatic islets of fetuses from diabetic rats

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PREVENTION AND REVERSAL DESPITE HYPERGLYCEMIA OF GLYCOGEN INFILTRATION (“HYDROPIC DEGENERATION”) IN THE PANCREAS IN ALLOXAN DIABETES IN THE RABBIT¹