Related Experiment Video

Updated: Jul 28, 2026

A Model of Chronic Nutrient Infusion in the Rat
08:18

A Model of Chronic Nutrient Infusion in the Rat

Published on: August 14, 2013

5-thio-D-glucose elevates renal transforming growth factor beta-1 at a dose that does not prevent streptozocine

P H Lane1

  • 1Department of Pediatrics, University of Nebraska Medical Center, Omaha 68198-2169, USA. phlane@unmc.edu

Endocrinology
|August 31, 2000
PubMed

Insights

5-thio-D-glucose (5TG) did not effectively control diabetes in rats and unexpectedly increased kidney transforming growth factor beta1 (TGF-beta1). Therefore, 5TG is unsuitable as a control for studying diabetic nephropathy in streptozocin (STZ)-induced diabetes models.

Area of Science:

  • Nephrology
  • Endocrinology
  • Biochemistry

Background:

  • Diabetic nephropathy studies using streptozocin (STZ) are hindered by STZ's inherent nephrotoxicity.
  • Previous research on STZ's diabetogenic effects has not fully evaluated potential kidney impacts of its inhibitors.

Purpose of the Study:

  • To investigate the effects of 5-thio-D-glucose (5TG), an inhibitor of STZ's diabetogenic actions, on renal hypertrophy and transforming growth factor beta1 (TGF-beta1) in STZ-treated rats.
  • To assess the suitability of 5TG as a control agent in models of STZ-induced diabetic nephropathy.

Main Methods:

  • Forty male Sprague Dawley rats were divided into four groups: saline control (SC), 5TG alone, 5TG + STZ, and STZ.
  • Animals were observed for two weeks, followed by analysis of urine, plasma, and kidney tissues.
  • Messenger RNA (mRNA) and protein levels of active and total TGF-beta1 were quantified.

Main Results:

  • STZ induced diabetes in 90% of rats; 5TG + STZ resulted in diabetes in 50% of rats.
  • Both STZ and 5TG + STZ groups showed elevated TGF-beta1 mRNA and protein levels compared to SC.
  • 5TG alone also increased TGF-beta1 mRNA and protein levels, though to a lesser extent than STZ treatments.

Conclusions:

  • 5-thio-D-glucose (5TG) is not an effective or appropriate control for studying diabetic nephropathy in STZ-treated rats due to its limited efficacy and induction of renal TGF-beta1.
  • Further research could explore 5TG's potential in understanding the regulation of renal TGF-beta1 expression and excretion independently of diabetes.

More Related Videos

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes08:03

Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes

Published on: June 25, 2017

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively manages...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...