Exenatide Alters Gene Expression of Neural Cell Adhesion Molecule (NCAM), Intercellular Cell Adhesion Molecule (ICAM), and Vascular Cell Adhesion Molecule (VCAM) in the Hippocampus of Type 2 Diabetic Model Mice

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Abstract

Background

Glucagon-like peptide-1 (GLP-1), a potent and selective agonist for the GLP-1 receptor, ameliorates the symptoms of diabetes through stimulation of insulin secretion. Exenatide is a potent and selective agonist for the GLP-1 receptor. Cell adhesion molecules are members of the immunoglobulin superfamily and are involved in synaptic rearrangements in the mature brain.

Material/Methods

The present study demonstrated the effects of exenatide treatment (0.1 μg/kg, subcutaneously, twice daily for 2 weeks) on the gene expression levels of cell adhesion molecules, neural cell adhesion molecule (NCAM), intercellular cell adhesion molecule (ICAM), and vascular cell adhesion molecule (VCAM) in the brain tissue of diabetic BALB/c male mice by real-time quantitative polymerase chain reaction (PCR). Diabetes was induced by streptozotocin/nicotinamide (STZ-NA) injection to male mice.

Results

The results of this study revealed that hippocampal gene expression of NCAM, ICAM, and VCAM were found to be up-regulated in STZ-NA-induced diabetic mice compared to those of controls. A significant decrease in the gene expression levels of NCAM, ICAM, and VCAM were determined after 2 weeks of exenatide administration.

Conclusions

Cell adhesion molecules may be involved in the molecular mechanism of diabetes. Exenatide has a strong beneficial action in managing diabetes induced by STZ/NA by altering gene expression of NCAM, ICAM, and VCAM.

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Most cited references 38

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A major role for VCAM-1, but not ICAM-1, in early atherosclerosis.

M Cybulsky, K Iiyama, H. Li … (2001)

VCAM-1 and ICAM-1 are endothelial adhesion molecules of the Ig gene superfamily that may participate in atherogenesis by promoting monocyte accumulation in the arterial intima. Both are expressed in regions predisposed to atherosclerosis and at the periphery of established lesions, while ICAM-1 is also expressed more broadly. To evaluate functions of VCAM-1 in chronic disease, we disrupted its fourth Ig domain, producing the murine Vcam1(D4D) allele. VCAM-1(D4D) mRNA and protein were reduced to 2-8% of wild-type allele (Vcam1(+)) levels but were sufficient to partially rescue the lethal phenotype of VCAM-1-null embryos. After crossing into the LDL receptor-null background, Vcam1(+/+) and Vcam1(D4D/D4D) paired littermates were generated from heterozygous intercrosses and fed a cholesterol-enriched diet for 8 weeks. The area of early atherosclerotic lesions in the aorta, quantified by en face oil red O staining, was reduced significantly in Vcam1(D4D/D4D) mice, although cholesterol levels, lipoprotein profiles, and numbers of circulating leukocytes were comparable to wild-type. In contrast, deficiency of ICAM-1 either alone or in combination with VCAM-1 deficiency did not alter nascent lesion formation. Therefore, although expression of both VCAM-1 and ICAM-1 is upregulated in atherosclerotic lesions, our data indicate that VCAM-1 plays a dominant role in the initiation of atherosclerosis.

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The rising global burden of diabetes and its complications: estimates and projections to the year 2010.

P Zimmet, Sarah-Beth Amos, D McCarty (1996)

Prevention and control programmes are needed to stem the rising epidemic of diabetes and its complications. However, these will not occur unless governments and public health planners are aware of the potential problem. Using published prevalence rates for NIDDM in different populations, and the current and projected age distributions, worldwide prevalence of NIDDM was estimated for 1995 and 1997, and well as projections for 2000 and 2010. Prevalence rates used for projections were chosen to reflect changes in lifestyle with economic development. The global prevalence of IDDM was estimated using published incidence rates and population figures, incorporating the likely survival time from development of IDDM. Data on diabetes complications are also summarised but no attempt has been made to extrapolate to a global estimated. In 1997, an estimated 124 million people worldwide have diabetes, 97% of these having NIDDM. By the year 2010 the total number of people with diabetes is projected to reach 221 million. The regions with the greatest potential increases are Asia and Africa, where diabetes rates could rise to 2 or 3 times those experienced today. With improvements in the treatment of IDDM, the prevalence of this form of diabetes is likely to increase as more people survive for longer after diagnosis. Increases in complications will undoubtedly follow increasing prevalence of diabetes, but population-based studies using standardised methods of diagnosis are required before reliable estimates of the extent of the problem can be made. It is hoped that the information provided in this report, and others like it, will act as an incentive to initiate or improve local diabetes monitoring and prevention strategies.

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Tissue-specific expression of the human receptor for glucagon-like peptide-I: brain, heart and pancreatic forms have the same deduced amino acid sequences.

Y Wei, S Mojsov (1995)

Glucagon-like peptide-I(GLP-I), encoded by the glucagon gene and released from the gut in response to nutrients, is a potent stimulator of glucose-induced insulin secretion. In human subjects GLP-I exerts its physiological effect as an incretin. The incretin effect of GLP-I is preserved in patients with Type II diabetes mellitus (NIDDM), suggesting that GLP-I receptor agonist can be used therapeutically in this group of patients. In these studies we addressed the question of whether GLP-I has broader actions in human physiology. To investigate this issue we examined the tissue distribution of GLP-I receptor using RNAse protection assay in order to avoid the cross-reactivities with structurally related receptors and to increase the sensitivity of detection. The riboprobe was synthesized from the human pancreatic GLP-I receptor cDNA and used in hybridization experiments with total RNA isolated from different human tissues. In addition to the pancreas, we found expression of GLP-I receptor mRNA in lung, brain, kidney, stomach and heart. Peripheral tissues which are the major sites of glucose turnover, such as liver, skeletal muscle and adipose did not express the pancreatic form of the GLP-I receptor. We also cloned and sequenced GLP-I receptor cDNA from human brain and heart. The deduced amino acid sequences are the same as the sequence found in the pancreas. These results indicate that GLP-I might have effects beyond the pancreas, including the cardiovascular and central nervous systems where a receptor with the same ligand binding specificity is found.

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Author and article information

Journal

Journal ID (nlm-ta): Med Sci Monit

Journal ID (iso-abbrev): Med. Sci. Monit

Journal ID (publisher-id): Medical Science Monitor

Title: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

Publisher: International Scientific Literature, Inc.

ISSN (Print): 1234-1010

ISSN (Electronic): 1643-3750

Publication date Collection: 2016

Publication date (Electronic): 28 July 2016

Volume: 22

Pages: 2664-2669

Affiliations

[1 ]Department of Genetics, Kocaeli University, Medical Faculty, Kocaeli, Turkey

[2 ]Department of Pharmacology, Kocaeli University, Medical Faculty, Kocaeli, Turkey

Author notes

Corresponding Author: Oguz Mutlu, e-mail: oguzmutlu80@ 123456hotmail.com

[A]

Study Design

[B]

Data Collection

[C]

Statistical Analysis

[D]

Data Interpretation

[E]

Manuscript Preparation

[F]

Literature Search

[G]

Funds Collection

Article

Publisher ID: 897401

DOI: 10.12659/MSM.897401

PMC ID: 4975365

PubMed ID: 27465247

SO-VID: 29f0b101-0cc2-497d-9108-0978db737071

License:

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License

Exenatide Alters Gene Expression of Neural Cell Adhesion Molecule (NCAM), Intercellular Cell Adhesion Molecule (ICAM), and Vascular Cell Adhesion Molecule (VCAM) in the Hippocampus of Type 2 Diabetic Model Mice

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Abstract

Background

Material/Methods

Results

Conclusions

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Vascular Biology

Most cited references 38

A major role for VCAM-1, but not ICAM-1, in early atherosclerosis.

The rising global burden of diabetes and its complications: estimates and projections to the year 2010.

Tissue-specific expression of the human receptor for glucagon-like peptide-I: brain, heart and pancreatic forms have the same deduced amino acid sequences.

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