Lipoatrophic Diabetes-Associated Utero-Ovarian Dysfunction: Influence of Cellular Lipid Deposition on Norepinephrine Indices

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Abstract

Objective: Elucidation of the intracellular lipoatrophic diabetic state and the concomitant alterations in norepinephrine (NE) parameters characterizing female reproductive failure. Methods: Quantitation of intrinsic NE levels in utero-ovarian and pancreatic tissue samples of C57BL/KsJ (+/?) control and (db/db) diabetic littermate mice was by high performance liquid chromatography (HPLC) and compared with the microspectrofluorometric histofluorescent (HF) localization of cellular and parenchymal NE. Results: Diabetes-associated elevations in HPLC-detectable tissue NE concentrations occurred in all pancreatic and reproductive tract tissue samples as compared to control-matched samples, whereas concurrent HF analysis revealed suppressed perivascular and parenchymal NE depositions in diabetic mice. Conclusions: These data suggest that progressive hypertriglyceridemia/lipidemia may suppress the effectiveness of intrinsic elevations in tissue NE concentrations from effectively counterregulating the deleterious effects of the hyperglycemic, type-2 diabetic condition.

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Morphometric analysis of obesity (ob/ob)- and diabetes (db/db)-associated hypothalamic neuronal degeneration in C57BL/KsJ mice.

David Garris (1989)

The influence of the obese (ob/ob) and diabetes (db/db) genetic mutations on hypothalamic structure was investigated in C57BL/KsJ and C57BL/6J mice strains by morphometric analysis of medial basal nuclei which are recognized to possess glucoregulatory neurons. Brains were collected and prepared for histomorphometric analysis at selected times following the development of expressed obesity and diabetes (Type II, non-insulin dependent) syndromes in order to compare both the strain and genomic influences on neuronal viability in the hypothalamic ventromedial (VMH) and arcuate (ARC) nuclei of mutant and age-matched control mice. The severity of each syndrome was determined by monitoring the concomitant changes in body weight and blood glucose levels in all groups. Both (db/db) and (ob/ob) mutant C57BL/KsJ mice exhibited an increase in the number and distribution of degenerated neurons in the VMH and ARC nuclei relative to corresponding controls. The mutation-associated exacerbation of the normal age-related neuronal loss, as observed in control MBH nuclei, was temporally associated with the overt expression of the hyperglycemic component of the obese and diabetes syndromes in aging C57BL/KsJ mice. No temporal or causal relationships were noted between the enhanced rate of premature neuronal degeneration, and either body weight or blood glucose levels, in either (db/db) or (ob/ob) C57BL/6J mice relative to controls. These data suggest that the hyperglycemic condition which characterizes the (ob/ob) and (db/db) mutant C57BL/KsJ mice is causally associated with the pronounced, premature MBH neuronal degeneration in these mouse strains. Neuronal changes were not pronounced when the genetic mutations were expressed in C57BL/6J mice. The accompanying alterations in brain glucose metabolism, hormone sensitivity, bioamine content and function which are recognized to occur in these mutant C57BL/KsJ mice may be causally associated consequences of the observed changes in MBH structural integrity and neuronal competence, with the severity of the mutation-associated changes being related to genetic background of the murine strain.

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Estrogenic Stimulation of Hypothalamic-Limbic System Metabolism in Ageing Diabetic C57BL/KsJ Mice

David Garris (1999)

The therapeutic influences of estrogen treatment on age- and diabetes-related declines in regional brain glucose utilization (RBGU) rates were evaluated in 8- to 20-week-old female C57BL/KsJ normal (+/?) and diabetic (db/db) mice. Following either oil vehicle (oil: 0.1 ml) or estradiol (E: 1 µg/3.5 days) treatments starting at 3 weeks of age, RBGU rates were subsequently determined at 8, 12, 16 and 20 weeks of age. A gradual decline in the basal rate of brain glucose utilization was observed in all control (oil- and E-treated) groups between 8 and 20 weeks. Expression of the hyperglycemic-obese diabetes syndrome in db/db mice resulted in a significant reduction in RBGU rates between 8 and 20 weeks relative to control values. In estrogen-sensitive hypothalamic, septal and amygdaloid regions, E therapy modulated RBGU rates in db/db mice relative to oil-treated diabetics, but did not significantly alter utilization rates in +/? mice. In cortical samples, E therapy had no significant influence on glucose utilization rates in either control or diabetic groups. A noticeable pattern of maturation-associated decline in CNS glucose utilization rates in all brain regions resulted in comparable regional metabolic indices being exhibited by all groups at 20 weeks of age, with the exception of the diabetes-associated exacerbation of RBGU rates in the oil-treated db/db group. These data demonstrate that the normal development-related decline in regional brain carbohydrate metabolism is accelerated by the diabetes syndrome, and that E therapy can modulate the syndrome-associated suppression of glucose utilization in steroid-sensitive CNS loci. These data suggest that the depressive influences of the diabetes syndrome on brain carbohydrate utilization rates may be therapeutically modified in recognized CNS regions possessing steroid-sequestering, metabolically responsive neurons.

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Age- and diabetes-associated alterations in regional brain norepinephrine concentrations and adrenergic receptor populations in C57BL/KsJ mice

David Garris (1990)

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Author and article information

Journal

Journal ID (publisher-id): HRE

Journal ID (nlm-ta): Horm Res Paediatr

Journal ID (doi): 10.1159/issn.1663-2818

Title: Hormone Research in Paediatrics

Publisher: S. Karger AG

ISSN (Print): 1663-2818

ISSN (Electronic): 1663-2826

Publication date Subscription-year: 2002

Publication date (Print): 2002

Publication date (Electronic): 04 September 2002

Volume: 58

Issue: 3

Pages: 120-127

Affiliations

Division of Cell Biology and Biophysics, School of Biological Sciences and School of Medicine, University of Missouri-KansasCity,Mo., USA

Article

Publisher ID: 63579 Other ID: Horm Res 2002;58:120–127

DOI: 10.1159/000063579

PubMed ID: 12218377

SO-VID: d2dbc0fc-9644-45b0-bfc2-5bb3c0a255ae

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 15 August 2001

Date accepted : 17 April 2002

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Figures: 7, References: 20, Pages: 8

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Lipoatrophic Diabetes-Associated Utero-Ovarian Dysfunction: Influence of Cellular Lipid Deposition on Norepinephrine Indices

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Karger: Endocrinology

Most cited references 5

Morphometric analysis of obesity (ob/ob)- and diabetes (db/db)-associated hypothalamic neuronal degeneration in C57BL/KsJ mice.

Estrogenic Stimulation of Hypothalamic-Limbic System Metabolism in Ageing Diabetic C57BL/KsJ Mice

Age- and diabetes-associated alterations in regional brain norepinephrine concentrations and adrenergic receptor populations in C57BL/KsJ mice

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