Klein, H. H.

Matthaei, S.

Scriba, Peter Christian

English

Universität München: Elektronischen Publikationen

mm 
XIII CONGRESS OF THE INTERNATIONAL DIABETES FEDERATION 
Hosted by Diabetes Australia 
SUPPLEMENT 1 to Vol. 5, 1988 
ABSTRACTS 
Elsevier Science Publishers B.V. - Amsterdam 
© 1988, Elsevier Science Publishers B.V. (Biomedical Division) 
All rights rescrved. N o pari of ihis publication may be reproduced, stored in a retricval syslcm, or transmitted in any 
form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior written permission 
of the Publisher, Elsevier Science Publishers B.V. (Biomedical Division), P.O. Box 1527, 1000 BM Amsterdam, The 
Netherlands. 
N o responsibility is assumed by the Publisher for any injury and/or damage to persons or properly as a matter of 
produets liability, negligence or otherwise, or from any use or Operation of any methods, produets. instruetions or ideas 
contained in the material herein. Because of the rapid advances in the medical sciences, the Publisher recommends that 
independent verification of diagnoses and drug dosages should be made. 
Although all advertising material is expected to conform to ethical (medical) Standards, inclusion in this publication does 
not constitute a guarantee or endorsement of the quality or value of such produet or of the Claims made of it by its 
manufacturer. 
Special regulation.s for authors. Upon aeeeptance of an article by the Journal, the author(s) will be asked to transfer 
Copyright of the article to the Publisher. This transfer will ensure the widest possible dissemination of Information. 
Submission of a paper to this Journal entails the author's irrevocable and exclusivc authorization of the Publisher to 
collect any sums or consideralions for copying or reproduetion payable by third parties (as mentioned in Article 17, 
Paragraph 2 of the Dutch Copyright Act of 1912. and in the Royal Decree of June 20. 1974 (S. 351) pursuant to Article 
16b of the Dutch Copyright Act of 1912) and/or to act in or out of Court in connection therewith. 
Special regulation.s for rcaclers in die U.S.A. This Journal has been registered with the Copyright Clearance Center, Inc. 
Consent is given for copying of articles for personal or internal use, or for the personal use of specific clients. This consent 
is given on the condition that the copier pays through the Center the per-copy fee staled in the code on the fiist page of 
each article for copying beyond that permitted by Sections 107 or 108 of the U.S. Copyright Law. The appropriatc fee 
should be forwarded with a copy of the first page of the article to the Copyright Clearance Center, Inc.. 27 Congress 
Street, Salem, M A 01970, U.S.A. If no code appears in an article the author has not given broad consent to copy and 
permission to copy must be obtained directly from the author. All articles published prior to 1980 may be copied for a 
per-copy fee of USS 2.25, also payable through the Center. This consent does not exlcnd to other kinds of copying such 
as for general distribution, resale, advertising and promotion purposes. or for crealing new collective works. Special 
written permission must be obtained from the Publisher for such copying. 
Printed in The Nethcrlands 
INTRODUCTION 
This book contains the submitted abstracts for the oral and poster free Communications accepted for 
presentation at the 13th Congress of the International Diabetes Federation. The abstracts have been 
reproduced in the form in which they were submitted. 
Abstracts for plenary lectures and symposia are not included. The manuscripts of these presentations 
will be published in the Proceedings of the Congress which may be ordered at the Elsevier desk at the 
Congress. 
The book is arranged with the oral free Communications at the front followed by the poster free 
Communications. The abstracts are arranged and indexed according to the Session in which they are 
presented. For example, ORA-015-003 refers to the third presentation in session of 15 of the oral free 
Communications and POS-003-172 refers to poster 172 in the third poster session. The poster 
presentation number also represents the poster board number, ie POS-003-172 will appear on poster 
board No. 172. For convenience, a preliminary programme is included in this book. The final 
Programme, which may contain some minor alterations, is included in the programme booklet in your 
satchel. 
Programme and Publications Committees 
13th IDF Congress 
C O N T E N T S 
Introduction vii 
Programme xiii 
Oral Sessions 
Epidemiology of diabetes 
(ORA-001-001 - ORA-001-008) S3 
Diabetic nephropathy 
(ORA-002-001 - ORA-002-008) S7 
Insulin: Gene expression/Synthesis /Secret ion 
(ORA-003-001 - ORA-003-008) S i l 
Diet and oral agents in diabetes therapy 
(ORA-004-001 - ORA-004-008) S15 
Practical aspects of health care delivery in diabetes 
(ORA-005-001 - ORA-005-008) S19 
Insulin therapy 
(ORA-006-001 - ORA-006-008) S23 
Entero-pancreatic hormones 
(ORA-007-001 - ORA-007-008) S27 
Basic mechanisms of diabetic complications 
(ORA-008-001 - ORA-008-008) S31 
Lipids, atherosclerosis and diabetes 
(ORA-009-001 - ORA-009-008) S35 
Insulin receptors and mechanisms of insulin action - I 
(ORA-010-001 - ORA-010-008) S39 
Diabetes education 
(ORA-011-001 - ORA-011-008) S43 
Immuno therapy and pancreatic transplantation 
(ORA-012-001 - ORA-012-008) S47 
Pathogenesis of Type I diabetes 
(ORA-013-001 - ORA-013-008) S51 
Diabet ic neuropathy 
(ORA-014-001 - ORA-014-008) S55 
Insulin receptors and mechanisms of insulin action - II 
(ORA-015-001 - ORA-015-008) S59 
Growth h o r m o n e / I G F 
(ORA-016-001 - ORA-016-008) S63 
Diabetic retinopathy 
(ORA-017-001 - ORA-017-008) S67 
Glucose metabolism in vitro and in vivo 
(ORA-018-001 - ORA-018-008) S71 
Poster Sessions 
G u t hormones and diabetes 
(POS-001-001 - POS-001-006) S77 
Glucagon and somatostatin 
(POS-001-007 - POS-001-024) S80 
Catecholamines 
(POS-001-025 - POS-001-033) S89 
Growth h o r m o n e s / I G F 
(POS-001-034 - POS-001-051) S94 
Insulin synthesis and gene expression 
(POS-001-052 - POS-001-057) S103 
Insulin secretion I 
(POS-001-058 - POS-001-075) S106 
Metabolism I: In vivo 
(POS-001-076 - POS-001-102) S115 
Pathogenesis of Type I diabetes I 
(POS-001-103 - POS-001-130) S129 
Diabetic complications I 
(POS-001-131 - POS-001-151) S143 
Lipids I 
(POS-001-152 - POS-001-166) S154 
Insulin therapy I 
(POS-001-167 - POS-001-191) S162 
Immunotherapy 
(POS-001-192 - POS-001-209) S175 
Genetics of diabetes 
(POS-001-210 - POS-001-232) S184 
Atherosclerosis in diabetes - Basic mechanisms 
(POS-001-233 - POS-001-245) S196 
Epidemiology I 
(POS-001-246 - POS-001-264) S203 
Health care I 
(POS-001-265 - POS-001-283) S213 
Insulin secretion II 
(POS-002-001 - POS-002-013) S223 
Insulin receptors /Mechanisms of insulin action I 
(POS-002-014 - POS-002-037A) S230 
Metabolism II: In vitro 
(POS-002-038 - POS-002-047) S243 
Pathogenesis of Type I diabetes II 
(POS-002-048 - POS-002-076) S248 
Aetiology of Type II diabetes 
(POS-002-077 - POS-002-097) S263 
Quantitative approaches to metabolism 
(POS-002-098 - POS-002-105) S274 
Diabetic complications II 
(POS-002-106 - POS-002-128A) S278 
Diabetic compl ica t ions /Re t inopa thy I 
(POS-002-129 - POS-002-146) S290 
Diabetic nephropathy I 
(POS-002-147 - POS-002-164A) S299 
Neuropathy I 
(POS-002-165 - POS-002-182) S309 
Diet and oral therapy I 
(POS-002-183 - POS-002-200) S318 
Pancreas transplantat ion 
(POS-002-201 - POS-002-221) S327 
Epidemiology II 
(POS-002-222 - POS-002-241) S338 
Health care II 
(POS-002-242 - POS-002-258) S348 
Insulin secretion in vivo I 
(POS-003-001 - POS-003-017) S357 
Insulin receptors /Mechanisms of insuhn action II 
(POS-003-018 - POS-003-041) S366 
Animal models of diabetes I 
(POS-003-042 - POS-003-061) S378 
Nutrit ion and obesity 
(POS-003-062 - POS-003-084) S388 Ketogenesis and ketoacidosis 85 90 400
Glycosylation 
(POS-003-091 - POS-003-114) S403 
Diabetic compl ica t ions /Basic mechanisms I 
(POS-003-115 - POS-003-136) S415 
Diabetic nephropathy II 
(POS-003-137 - POS-003-154) S426 
Neuropathy II 
(POS-003-155 - POS-003-174) S435 
Lipids II 
(POS-003-175 - POS-003-190) S445 
Pregnancy and diabetes 
(POS-003-191 - POS-003-219) S453 
Insuün therapy II 
(POS-003-220 - POS-003-240) S468 
Diet and oral therapy II 
(POS-003-241 - POS-003-260) S479 
Epidemiology III 
(POS-003-261 - POS-003-278) S489 
Diabetes education I 
(POS-003-279 - POS-003-294) S498 
Insulin secretion in vivo II 
(POS-004-001 - POS-004-012) S506 
Insuün receptors /Mechanisms of insulin action III 
(POS-004-013 - POS-004-026) S512 
Neural control 
(POS-004-027 - POS-004-039) S519 
Animal models of diabetes II 
(POS-004-040 - POS-004-055) S526 
Exercise 
(POS-004-056 - POS-004-066) S534 
Diabetes control 
(POS-004-067 - POS-004-086) S540 
Diabetic complicat ions/Basic mechanisms II 
(POS-004-087 - POS-004-106) S550 
Diabetic compl ica t ions /Ret inopathy II 
(POS-004-107 - POS-004-121) S560 
Diabetic nephropathy III 
(POS-004-122 - POS-004-137) S568 
Neuropathy III 
(POS-004-138 - POS-004-156) S576 
Atherosclerosis, hypertension and diabetes 
(POS-004-157 - POS-004-184) S586 
Insulin therapy III 
(POS-004-185 - POS-004-207) S600 
Diet and oral therapy III 
(POS-004-208 - POS-004-226) S612 
Clinical hypoglycaemia 
(POS-004-227 - POS-004-244) S622 
Epidemiology IV 
(POS-004-245 - POS-004-263) S631 
Diabetes education II 
(POS-004-264 - POS-004-277) S641 
Psychological and behavioral aspects of diabetes 
(POS-004-278 - POS-004-293) S648 
Author index S657 
POS-002-024 
ISOPROTERENOL DECREASES ACTIVATION BY INSULIN OF INSULIN RECEPTOR KINASE 
IN INTACT RAT ADIPOCYTES. 
H.H. KLEIN1, S. MATTHAEI2, P.C. SCRIBA1 
Departments of Internal Medicine^University of Lübeck and 2University of Hamburg, FRG. 
It has been previously shown that ß-adrenergic agonists produce insulin(I)-resistance 
both in vivo and in vitro. We have studied the effect of isoproterenol(ISO) on I-binding 
and activation of insulin receptor kinase(IRK) in intact rat adipocytes. Cell concentra-
tion was <2xl03/ml in buffer containing 2%BSA and 40mM Hepes (pH 7.4). Preincubation with 
ISO (ltyiM) was for 30min at 37<>C. l 2 s I - I was then added to a fraction of the cells for 
15min at 37°C to measure I-binding. The other cells were exposed to various concentra-
tions of I for 15min at 37°C in order to activate the cellular IRK. IRK was then isolated 
and immunoprecipitated in the presence of Phosphatase inhibitors. Under these conditions, 
IRK-activity that resulted from exposure to insulin while the cells were intact, was pre-
served. It was subsequently measured in the presence of 0.5 /iM 32P-ATP and lmg/ml histone 
and was (fmol P into histone/pmol I-binding activity/min): 
Insulin(ng/ml): 0 4 20 500 
-ISO : 4.6+1.0 30.5+5.1 93.8+11.6 124.8+39.3 
+ISO : 4.3+1.1 22.8+2.5 66.1+ 1.0 112.0+27.8 
Mean values for trace I-binding to the cells were: -ISO:0,49+0.12; +180:0,45+0.08%. 
Conclusions: (1)Exposure of the cells to insulin stimulated IRK-activity 25-30fold. 
(2) Activation of IRK by I in intact cells was reduced up to 30% in the presence of ISO. 
(3) Only a minimal, i f any, reduction of I-binding to the cells was observed in the pre-
sence of ISO. (4)0ur data thus suggest that ISO reduces I-activation of IRK in intact 
cells on a post-binding level. 
S235 


Isoproterenol decreases activation by insulin of insulin receptor kinase in intact rat adipocytes

Open Access LMU

mm XIII CONGRESS OF THE INTERNATIONAL DIABETES FEDERATION Hosted by Diabetes Australia SUPPLEMENT 1 to Vol. 5, 1988 ABSTRACTS Elsevier Science Publishers B.V. - Amsterdam © 1988, Elsevier Science Publishers B.V. (Biomedical Division) All rights rescrved. N o pari of ihis publication may be reproduced, stored in a retricval syslcm, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior written permission of the Publisher, Elsevier Science Publishers B.V. (Biomedical Division), P.O. Box 1527, 1000 BM Amsterdam, The Netherlands. N o responsibility is assumed by the Publisher for any injury and/or damage to persons or properly as a matter of produets liability, negligence or otherwise, or from any use or Operation of any methods, produets. instruetions or ideas contained in the material herein. Because of the rapid advances in the medical sciences, the Publisher recommends that independent verification of diagnoses and drug dosages should be made. Although all advertising material is expected to conform to ethical (medical) Standards, inclusion in this publication does not constitute a guarantee or endorsement of the quality or value of such produet or of the Claims made of it by its manufacturer. Special regulation.s for authors. Upon aeeeptance of an article by the Journal, the author(s) will be asked to transfer Copyright of the article to the Publisher. This transfer will ensure the widest possible dissemination of Information. Submission of a paper to this Journal entails the author's irrevocable and exclusivc authorization of the Publisher to collect any sums or consideralions for copying or reproduetion payable by third parties (as mentioned in Article 17, Paragraph 2 of the Dutch Copyright Act of 1912. and in the Royal Decree of June 20. 1974 (S. 351) pursuant to Article 16b of the Dutch Copyright Act of 1912) and/or to act in or out of Court in connection therewith. Special regulation.s for rcaclers in die U.S.A. This Journal has been registered with the Copyright Clearance Center, Inc. Consent is given for copying of articles for personal or internal use, or for the personal use of specific clients. This consent is given on the condition that the copier pays through the Center the per-copy fee staled in the code on the fiist page of each article for copying beyond that permitted by Sections 107 or 108 of the U.S. Copyright Law. The appropriatc fee should be forwarded with a copy of the first page of the article to the Copyright Clearance Center, Inc.. 27 Congress Street, Salem, M A 01970, U.S.A. If no code appears in an article the author has not given broad consent to copy and permission to copy must be obtained directly from the author. All articles published prior to 1980 may be copied for a per-copy fee of USS 2.25, also payable through the Center. This consent does not exlcnd to other kinds of copying such as for general distribution, resale, advertising and promotion purposes. or for crealing new collective works. Special written permission must be obtained from the Publisher for such copying. Printed in The Nethcrlands INTRODUCTION This book contains the submitted abstracts for the oral and poster free Communications accepted for presentation at the 13th Congress of the International Diabetes Federation. The abstracts have been reproduced in the form in which they were submitted. Abstracts for plenary lectures and symposia are not included. The manuscripts of these presentations will be published in the Proceedings of the Congress which may be ordered at the Elsevier desk at the Congress. The book is arranged with the oral free Communications at the front followed by the poster free Communications. The abstracts are arranged and indexed according to the Session in which they are presented. For example, ORA-015-003 refers to the third presentation in session of 15 of the oral free Communications and POS-003-172 refers to poster 172 in the third poster session. The poster presentation number also represents the poster board number, ie POS-003-172 will appear on poster board No. 172. For convenience, a preliminary programme is included in this book. The final Programme, which may contain some minor alterations, is included in the programme booklet in your satchel. Programme and Publications Committees 13th IDF Congress C O N T E N T S Introduction vii Programme xiii Oral Sessions Epidemiology of diabetes (ORA-001-001 - ORA-001-008) S3 Diabetic nephropathy (ORA-002-001 - ORA-002-008) S7 Insulin: Gene expression/Synthesis /Secret ion (ORA-003-001 - ORA-003-008) S i l Diet and oral agents in diabetes therapy (ORA-004-001 - ORA-004-008) S15 Practical aspects of health care delivery in diabetes (ORA-005-001 - ORA-005-008) S19 Insulin therapy (ORA-006-001 - ORA-006-008) S23 Entero-pancreatic hormones (ORA-007-001 - ORA-007-008) S27 Basic mechanisms of diabetic complications (ORA-008-001 - ORA-008-008) S31 Lipids, atherosclerosis and diabetes (ORA-009-001 - ORA-009-008) S35 Insulin receptors and mechanisms of insulin action - I (ORA-010-001 - ORA-010-008) S39 Diabetes education (ORA-011-001 - ORA-011-008) S43 Immuno therapy and pancreatic transplantation (ORA-012-001 - ORA-012-008) S47 Pathogenesis of Type I diabetes (ORA-013-001 - ORA-013-008) S51 Diabet ic neuropathy (ORA-014-001 - ORA-014-008) S55 Insulin receptors and mechanisms of insulin action - II (ORA-015-001 - ORA-015-008) S59 Growth h o r m o n e / I G F (ORA-016-001 - ORA-016-008) S63 Diabetic retinopathy (ORA-017-001 - ORA-017-008) S67 Glucose metabolism in vitro and in vivo (ORA-018-001 - ORA-018-008) S71 Poster Sessions G u t hormones and diabetes (POS-001-001 - POS-001-006) S77 Glucagon and somatostatin (POS-001-007 - POS-001-024) S80 Catecholamines (POS-001-025 - POS-001-033) S89 Growth h o r m o n e s / I G F (POS-001-034 - POS-001-051) S94 Insulin synthesis and gene expression (POS-001-052 - POS-001-057) S103 Insulin secretion I (POS-001-058 - POS-001-075) S106 Metabolism I: In vivo (POS-001-076 - POS-001-102) S115 Pathogenesis of Type I diabetes I (POS-001-103 - POS-001-130) S129 Diabetic complications I (POS-001-131 - POS-001-151) S143 Lipids I (POS-001-152 - POS-001-166) S154 Insulin therapy I (POS-001-167 - POS-001-191) S162 Immunotherapy (POS-001-192 - POS-001-209) S175 Genetics of diabetes (POS-001-210 - POS-001-232) S184 Atherosclerosis in diabetes - Basic mechanisms (POS-001-233 - POS-001-245) S196 Epidemiology I (POS-001-246 - POS-001-264) S203 Health care I (POS-001-265 - POS-001-283) S213 Insulin secretion II (POS-002-001 - POS-002-013) S223 Insulin receptors /Mechanisms of insulin action I (POS-002-014 - POS-002-037A) S230 Metabolism II: In vitro (POS-002-038 - POS-002-047) S243 Pathogenesis of Type I diabetes II (POS-002-048 - POS-002-076) S248 Aetiology of Type II diabetes (POS-002-077 - POS-002-097) S263 Quantitative approaches to metabolism (POS-002-098 - POS-002-105) S274 Diabetic complications II (POS-002-106 - POS-002-128A) S278 Diabetic compl ica t ions /Re t inopa thy I (POS-002-129 - POS-002-146) S290 Diabetic nephropathy I (POS-002-147 - POS-002-164A) S299 Neuropathy I (POS-002-165 - POS-002-182) S309 Diet and oral therapy I (POS-002-183 - POS-002-200) S318 Pancreas transplantat ion (POS-002-201 - POS-002-221) S327 Epidemiology II (POS-002-222 - POS-002-241) S338 Health care II (POS-002-242 - POS-002-258) S348 Insulin secretion in vivo I (POS-003-001 - POS-003-017) S357 Insulin receptors /Mechanisms of insuhn action II (POS-003-018 - POS-003-041) S366 Animal models of diabetes I (POS-003-042 - POS-003-061) S378 Nutrit ion and obesity (POS-003-062 - POS-003-084) S388 Ketogenesis and ketoacidosis 85 90 400Glycosylation (POS-003-091 - POS-003-114) S403 Diabetic compl ica t ions /Basic mechanisms I (POS-003-115 - POS-003-136) S415 Diabetic nephropathy II (POS-003-137 - POS-003-154) S426 Neuropathy II (POS-003-155 - POS-003-174) S435 Lipids II (POS-003-175 - POS-003-190) S445 Pregnancy and diabetes (POS-003-191 - POS-003-219) S453 Insuün therapy II (POS-003-220 - POS-003-240) S468 Diet and oral therapy II (POS-003-241 - POS-003-260) S479 Epidemiology III (POS-003-261 - POS-003-278) S489 Diabetes education I (POS-003-279 - POS-003-294) S498 Insulin secretion in vivo II (POS-004-001 - POS-004-012) S506 Insuün receptors /Mechanisms of insulin action III (POS-004-013 - POS-004-026) S512 Neural control (POS-004-027 - POS-004-039) S519 Animal models of diabetes II (POS-004-040 - POS-004-055) S526 Exercise (POS-004-056 - POS-004-066) S534 Diabetes control (POS-004-067 - POS-004-086) S540 Diabetic complicat ions/Basic mechanisms II (POS-004-087 - POS-004-106) S550 Diabetic compl ica t ions /Ret inopathy II (POS-004-107 - POS-004-121) S560 Diabetic nephropathy III (POS-004-122 - POS-004-137) S568 Neuropathy III (POS-004-138 - POS-004-156) S576 Atherosclerosis, hypertension and diabetes (POS-004-157 - POS-004-184) S586 Insulin therapy III (POS-004-185 - POS-004-207) S600 Diet and oral therapy III (POS-004-208 - POS-004-226) S612 Clinical hypoglycaemia (POS-004-227 - POS-004-244) S622 Epidemiology IV (POS-004-245 - POS-004-263) S631 Diabetes education II (POS-004-264 - POS-004-277) S641 Psychological and behavioral aspects of diabetes (POS-004-278 - POS-004-293) S648 Author index S657 POS-002-024 ISOPROTERENOL DECREASES ACTIVATION BY INSULIN OF INSULIN RECEPTOR KINASE IN INTACT RAT ADIPOCYTES. H.H. KLEIN1, S. MATTHAEI2, P.C. SCRIBA1 Departments of Internal Medicine^University of Lübeck and 2University of Hamburg, FRG. It has been previously shown that ß-adrenergic agonists produce insulin(I)-resistance both in vivo and in vitro. We have studied the effect of isoproterenol(ISO) on I-binding and activation of insulin receptor kinase(IRK) in intact rat adipocytes. Cell concentra-tion was <2xl03/ml in buffer containing 2%BSA and 40mM Hepes (pH 7.4). Preincubation with ISO (ltyiM) was for 30min at 37<>C. l 2 s I - I was then added to a fraction of the cells for 15min at 37°C to measure I-binding. The other cells were exposed to various concentra-tions of I for 15min at 37°C in order to activate the cellular IRK. IRK was then isolated and immunoprecipitated in the presence of Phosphatase inhibitors. Under these conditions, IRK-activity that resulted from exposure to insulin while the cells were intact, was pre-served. It was subsequently measured in the presence of 0.5 /iM 32P-ATP and lmg/ml histone and was (fmol P into histone/pmol I-binding activity/min): Insulin(ng/ml): 0 4 20 500 -ISO : 4.6+1.0 30.5+5.1 93.8+11.6 124.8+39.3 +ISO : 4.3+1.1 22.8+2.5 66.1+ 1.0 112.0+27.8 Mean values for trace I-binding to the cells were: -ISO:0,49+0.12; +180:0,45+0.08%. Conclusions: (1)Exposure of the cells to insulin stimulated IRK-activity 25-30fold. (2) Activation of IRK by I in intact cells was reduced up to 30% in the presence of ISO. (3) Only a minimal, i f any, reduction of I-binding to the cells was observed in the pre-sence of ISO. (4)0ur data thus suggest that ISO reduces I-activation of IRK in intact cells on a post-binding level. S235 

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Isoproterenol decreases activation by insulin of insulin receptor kinase in intact rat adipocytes

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