Related Experiment Video

Updated: Oct 8, 2025

Incorporation of a Survivable Liver Biopsy Procedure in Mice to Assess Non-alcoholic Steatohepatitis NASH Resolution
04:14

Incorporation of a Survivable Liver Biopsy Procedure in Mice to Assess Non-alcoholic Steatohepatitis NASH Resolution

Published on: April 16, 2019

12.2K

Liraglutide Inhibits Osteoclastogenesis and Improves Bone Loss by Downregulating Trem2 in Female Type 1 Diabetic

Jie Yu1, Yan-Chuan Shi2,3, Fan Ping1

  • 1Key Laboratory of Endocrinology of National Health Commission, Department of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

Frontiers in Endocrinology
|January 3, 2022
PubMed
Abstract

Insights

Type 1 diabetes (T1D) causes bone loss by increasing osteoclastogenesis. Liraglutide, a GLP-1 receptor agonist, protects bone in T1D mice by suppressing this process, offering a potential therapeutic strategy.

Area of Science:

  • Endocrinology
  • Bone Biology
  • Pharmacology

Background:

  • Type 1 diabetes (T1D) is associated with bone fragility, but the underlying mechanisms remain unclear.
  • The potential of glucagon-like peptide-1 receptor (GLP-1R) agonists to improve bone quality in T1D is not well-established.

Purpose of the Study:

  • To investigate the mechanisms of bone loss in T1D.
  • To determine the effects of liraglutide on bone quality in a mouse model of T1D using transcriptomics.

Main Methods:

  • Female mice with streptozotocin-induced T1D were treated with saline, insulin, liraglutide, or a combination for 8 weeks.
  • Transcriptomics analysis of tibia was performed on normal glucose tolerance (NGT), saline-treated T1D, and liraglutide-treated T1D groups.

Main Results:

  • T1D mice exhibited hyperglycemia, weight loss, reduced bone mineral density (BMD), and impaired microarchitecture.
  • Liraglutide treatment improved BMD and partially corrected microarchitectural defects.
  • Transcriptomics revealed upregulated genes related to osteoclastogenesis and inflammation in T1D mice, which were downregulated by liraglutide.

Conclusions:

  • Increased osteoclastogenesis, evidenced by upregulated Trem2 expression, contributes significantly to bone loss in T1D.
  • Liraglutide demonstrates protective effects against bone loss in T1D by suppressing osteoclastogenesis.
Keywords:
Triggering receptor expressed on myeloid cells 2bone densitybone lossbone microarchitectureliraglutideosteoclastogenesistranscriptomicstype 1 diabetes

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

7.5K
A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders11:47

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

Published on: June 8, 2014

11.9K

Related Concept Videos

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...
465
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...
280
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...
4.6K
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...
334
Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
3.1K