Data-Base Management System (DBMS) is the current standard for storing information. A DBMS organizes and maintains a structure of storage of data. Databases make it possible to store vast amounts of randomly created information and then retrieve items using associative reasoning in search routines. However, design of databases is cumbersome. If one is to use a database primarily to directly input information, each field must be predefined manually, and the fields must be organized to permit coherent data input. This static requirement is problematic and requires that database table(s) be predefined and customized at the outset, a difficult proposition since current DBMS lack a user friendly front end to allow flexible design of the input model. Furthermore, databases are primarily text based, making it difficult to process graphical data. We have developed a general and nonproprietary approach to the problem of input modeling designed to make use of the known informational architecture to map data to a database and then retrieve the original document in freely editable form. We create form templates using ordinary word processing software: Microsoft InfoPath 2007. Each field in the form is given a unique name identifier in order to be distinguished in the database. It is possible to export text based documents created initially in Microsoft Word by placing a colon at the beginning of any desired field location. InfoPath then captures the preceding string and uses it as the label for the field. Each form can be structured in a way to include any combination of both textual and graphical fields. We input data into InfoPath templates. We then submit the data through a web service to populate fields in an SQL database. By appropriate indexing, we can then recall the entire document from the SQL database for editing, with corresponding audit trail. Graphical data is handled no differently than textual data and is embedded in the database itself permitting direct query approaches. This technique makes it possible for general users to benefit from a combined text-graphical database environment with a flexible non-proprietary interface. Consequently, any template can be effortlessly transformed to a database system and easily recovered in a narrative form

Hormonal changes and estrogen deficiency accompanying menopause have several effects on women such as weight gain in the form of adipose tissue. An increase in adiposity associates with an increased production of leptin, an adipocyte derived hormone, that acts mainly in the central nervous system. Leptin regulates energy balance and plays a primary role in the regulation of glucose homeostasis. In this study, we aim to determine leptin's effect on renal glucose handling in an estrogen deficient adult female rat model (ovariectomized; OVX). We observed significant weight gain, increase in glomerular filtration rate (GFR, increase in creatinine clearance from 1.3 ml/min to 2.3 ml/min) and protein level of an early biomarker of kidney injury, the neutrophil gelatinase‐associated lipocalin (NGAL, 90% increase in both glomeruli and tubules, measured by immunohistochemistry) in OVX rats when compared to their sham‐operated controls. The mechanism proposed for the increase in GFR and renal damage is lipotoxicity due to intrarenal lipid accumulation associated with increased perirenal adipose tissue. Indeed, a significant accumulation of renal lipid, assessed using oil red O staining, was detected in the renal tubules of the OVX rats when compared with their controls. All these effects were partially reversed by treatment with a leptin receptor antagonist (LAN‐6, 3µg/day), delivered for four weeks into the lateral ventricle by an osmotic pump. The sodium‐glucose cotransporter‐2 (SGLT2), the main mediator of renal glucose handling, is co‐expressed in renal proximal tubules (PTs) with Na/H exchanger‐3 (NHE3), a key player of salt regulation. Using immunohistochemistry, we measured significant reduction of renal SGLT2 protein expression level in OVX rats when compared with their controls. NHE3 protein expression level was also decreased in the same PTs. The decrease in SGLT2 and NHE3 protein expression measured in OVX rats and glycosuria detected in the urine of OVX rats was significantly reduced in rats treated with LAN‐6. Serum glucose levels did not change significantly in the conditions under study. These findings suggest that in the absence of estrogen: 1. infiltration of renal lipid leads to renal injury, 2. kidney injury combines with an increase in GFR, 3. protein expression levels of SGLT2 and NHE3 are decreased and renal glycosuria develops. Finally, blocking activation of central leptin receptors in part restores kidney function. This may shed light in the understanding of leptin's regulation of glucose homeostasis and lead to potential benefits against kidney dysfunction caused by intrarenal lipid accumulation that develops during estrogen deficiency.

Women in menopause have substantial variations in hormonal balance. The weight gain in the form of adipose tissue in these women has been associated to an increase in leptin level; an adipocyte‐derived hormone that acts primarily on the central nervous system. The increase in central leptin has been related with the development of hypertension via an increase in renal sympathetic nerve activity (RSNA) and activation of RSNA has been demonstrated to play a role in the progression of kidney dysfunction. Therefore, we hypothesize that activation of RSNA due to elevated leptin induces hypertension via an action on kidney function. Utilizing a menopausal rat model, we studied the mechanisms mediated by central leptin receptor activation to alter kidney function. We measured the glomerular filtration rate (GFR) by creatinine clearance and protein level of the neutrophil gelatinase‐associated lipocalin (NGAL), an early biomarker of kidney injury, by immunohistochemistry. An increase in creatinine clearance (from 1.3 ml/min to 2.3 ml/min) and protein levels of NGAL (over 90% increase in both glomeruli and tubules) was measured in ovariectomized adult female rats when compared with their sham‐operated controls. Treatment with leptin reception antagonist (LAN‐6, 3μg/day), delivered for four weeks into the lateral ventricle by an osmotic pump, significantly attenuated these effects. Furthermore, we determined that intra‐abdominal and perirenal fat accumulation were both markedly higher in the same menopausal rat models. Perirenal fat accumulation has been associated with lipid accumulation in renal tissues and excess of intrarenal lipid is increasingly recognized to contribute to kidney injury through lipotoxicity. We found a significant accumulation of renal lipid, tested using oil red O staining, in the renal tubules of the ovariectomized animals when compared with their controls. The lipid accumulation was partially reversed by the leptin receptor antagonist treatment. In summary, the increase in GFR associated with kidney injury suggests the development of kidney disease in this rat model of menopause that is in part reversed by blocking central leptin receptors; infiltration of lipid in the renal tissue is proposed as a possible mechanism of kidney injury. These findings have the potential to translate into future therapeutic strategies for treating kidney injury in menopausal mediated‐hypertension.Support or Funding InformationIowa Osteopathic Education and Research FundsThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.