NDLI: Tat-modified leptin is more accessible to hypothalamus through brain-blood barrier with a significant inhibition of body-weight gain in high-fat-diet fed mice.

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Tat-modified leptin is more accessible to hypothalamus through brain-blood barrier with a significant inhibition of body-weight gain in high-fat-diet fed mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, C. Su, Z. Zhao, B. Qu, Q. Tan, Y. Cai, L. Li, X.
Description	Country affiliation: China Author Affiliation: Zhang C ( Engineering Research Center of Bioreactor and Pharmaceutical Development, Ministry of Education, Jilin Agricultural University, Changchun, China.)
Abstract	Obesity in human was found mainly due to the poor transportation of leptin through brain-blood barrier (BBB), called as leptin resistance. To produce a leptin capable of penetrating BBB, we have added Tat-PTD(9) to the C terminal of leptin to construct a fusion protein. The fusion Tat-leptin and native leptin genes were synthesized by single-step insertion of a polymerase chain reaction and expressed in Escherichia coli BL21 (Rosseta). The expressing products were purified and renatured by Ni-NTA affinity chromatography, and identified by the molecular size in SDS-PAGE gel and by its immunoreactivity to specific antibody with Western-blotting assay. To bio-functionally evaluate the fusion protein, Balb/c mice fed with high-fat diet (HFD) were given Tat-leptin, leptin or saline for 19 days. The immunohistochemical staining showed the increases in positive stains for the leptin in the region of hypothalamus of the HFD mice with either Tat-leptin or leptin as compared to saline group, but the staining intensity and frequency in the group with Tat-leptin were stronger and higher than those in the group with leptin. Furthermore, the most efficiency in preventing the body-weight gain caused by HFD was found in Tat-leptin group among these three groups. These results suggest that Tat-modified leptin may become a great potential candidate for the prevention or therapy of obese patients.
File Format	HTM / HTML
ISSN	09477349
Issue Number	1
Volume Number	118
e-ISSN	14393646
Journal	Experimental and Clinical Endocrinology & Diabetes
Language	English
Publisher	Thieme
Publisher Date	2010-01-01
Publisher Place	Germany
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Endocrinology Anti-obesity Agents Pharmacology Pharmacokinetics Hypothalamus Metabolism Leptin Analogs & Derivatives Peptide Fragments Tat Gene Products, Human Immunodeficiency Virus Animals Administration & Dosage Isolation & Purification Blood-brain Barrier Dietary Fats Drug Delivery Systems Methods Genes, Tat Drug Effects Pathology Immunohistochemistry Biosynthesis Genetics Male Mice Mice, Inbred Balb C Obesity Drug Therapy Polymerase Chain Reaction Random Allocation Recombinant Fusion Proteins Time Factors Tissue Distribution Weight Gain Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Endocrinology, Diabetes and Metabolism Internal Medicine Endocrinology

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