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Original Article
- Pharmacotherapy
- D2Rs Agonist Ropinirole Cooperates with Metformin to Modulate Thermogenesis and Ameliorate Obesity-Related Metabolic Disorders in Mice
- Bangrui Huang, Daowei Liu, Fakun Jiang, Zihui Wang, Chuanjun Mao, Qian Lu, Tao Chen, Chun Xie, Wenli Chen, Qian Wang, Wenyong Xiong
- Received April 14, 2025 Accepted October 4, 2025 Published online February 4, 2026
- DOI: https://doi.org/10.4093/dmj.2025.0335 [Epub ahead of print]
- 1,816 View
- 65 Download
- 1 Crossref
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Abstract
PDF
Supplementary Material
PubReader 
ePub - Background
Metabolic disorders represent a significant challenge to human health, primarily due to their widespread prevalence and the limited availability of alternative pharmacological interventions. Drug repurposing offers a promising and expedited strategy to address these conditions.
Methods
To elucidate the efficacy and underlying mechanism of the combination of metformin with ropinirole on anti-obesity and obesity-related metabolic disorders.
Results
The results indicate that the combination treatment led to a significant reduction in body weight and improvements in hyperglycemia, dyslipidemia, and insulin resistance. These enhancements, along with increased energy expenditure, were significantly greater than those achieved with either drug alone. Additionally, we observed the browning of inguinal white adipose tissue (iWAT) and alterations of the whitened-brown adipose tissue (BAT), along with substantial increases in mitochondrial function-related proteins. However, the drug combination did not exhibit any enhanced effect on cell thermogenesis and these proteins in vitro, whereas combination of norepinephrine and metformin-induced an additive upregulation of mitochondrial function-related proteins. Furthermore, pharmacological blockade of the β3 adrenergic receptor inhibited the energy expenditure induced by the combination treatment, etc.
Conclusion
Our study underscores the combination of metformin and ropinirole-induced an amplified effectiveness in treating obesity-related metabolic disorders is dependent on the dopamine-control sympathetic nerve activity, and metformin acts directly on BAT and iWAT to improve mitochondrial function, which offering a new perspective for future clinical co-treatment of metabolic disorders with these two drugs. -
Citations
Citations to this article as recorded by
- Metformin beyond Glycemic Control: New Mechanistic Insights and Expanding Therapeutic Horizons
Eugene Han, Jung Ho Nam, Insuk Lee, Cheol Ryong Ku, Yong-ho Lee
Diabetes & Metabolism Journal.2026; 50(3): 435. CrossRef
- Metformin beyond Glycemic Control: New Mechanistic Insights and Expanding Therapeutic Horizons
Reviews
- Basic Research
- Adipose Tissue and Metabolic Health
- Sung-Min An, Seung-Hee Cho, John C. Yoon
- Diabetes Metab J. 2023;47(5):595-611. Published online July 24, 2023
- DOI: https://doi.org/10.4093/dmj.2023.0011
- 62,059 View
- 1,882 Download
- 130 Web of Science
- 148 Crossref
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Abstract
PDFPubReader ePub
- In this review, we provide a brief synopsis of the connections between adipose tissue and metabolic health and highlight some recent developments in understanding and exploiting adipocyte biology. Adipose tissue plays critical roles in the regulation of systemic glucose and lipid metabolism and secretes bioactive molecules possessing endocrine, paracrine, and autocrine functions. Dysfunctional adipose tissue has a detrimental impact on metabolic health and is intimately involved in key aspects of metabolic diseases such as insulin resistance, lipid overload, inflammation, and organelle stress. Differences in the distribution of fat depots and adipose characteristics relate to divergent degrees of metabolic dysfunction found in metabolically healthy and unhealthy obese individuals. Thermogenic adipocytes increase energy expenditure via mitochondrial uncoupling or adenosine triphosphate-consuming futile substrate cycles, while functioning as a metabolic sink and participating in crosstalk with other metabolic organs. Manipulation of adipose tissue provides a wealth of opportunities to intervene and combat the progression of associated metabolic diseases. We discuss current treatment modalities for obesity including incretin hormone analogs and touch upon emerging strategies with therapeutic potential including exosome-based therapy, pharmacological activation of brown and beige adipocyte thermogenesis, and administration or inhibition of adipocyte-derived factors.
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- Diabetes Metab J. 2021;45(6):840-852. Published online June 25, 2021
- DOI: https://doi.org/10.4093/dmj.2020.0291
- 25,716 View
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Graphical Abstract
Abstract
PDFPubReader ePub - Brown adipose tissue (BAT) is a specialized tissue for nonshivering thermogenesis to dissipate energy as heat. Although BAT research has long been limited mostly in small rodents, the rediscovery of metabolically active BAT in adult humans has dramatically promoted the translational studies on BAT in health and diseases. Moreover, several remarkable advancements have been made in brown fat biology over the past decade: The molecular and functional analyses of inducible thermogenic adipocytes (socalled beige adipocytes) arising from a developmentally different lineage from classical brown adipocytes have been accelerated. In addition to a well-established thermogenic activity of uncoupling protein 1 (UCP1), several alternative thermogenic mechanisms have been discovered, particularly in beige adipocytes. It has become clear that BAT influences other peripheral tissues and controls their functions and systemic homeostasis of energy and metabolic substrates, suggesting BAT as a metabolic regulator, other than for thermogenesis. This notion is supported by discovering that various paracrine and endocrine factors are secreted from BAT. We review the current understanding of BAT pathophysiology, particularly focusing on its role as a metabolic regulator in small rodents and also in humans.
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Original Article
- Basic Research
-
- Ipragliflozin, an SGLT2 Inhibitor, Ameliorates High-Fat Diet-Induced Metabolic Changes by Upregulating Energy Expenditure through Activation of the AMPK/ SIRT1 Pathway
- Ji-Yeon Lee, Minyoung Lee, Ji Young Lee, Jaehyun Bae, Eugene Shin, Yong-ho Lee, Byung-Wan Lee, Eun Seok Kang, Bong-Soo Cha
- Diabetes Metab J. 2021;45(6):921-932. Published online February 22, 2021
- DOI: https://doi.org/10.4093/dmj.2020.0187
- 15,045 View
- 470 Download
- 39 Web of Science
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Graphical Abstract
Abstract
PDFSupplementary MaterialPubReader ePub
- Background
Sodium-glucose co-transporter 2 (SGLT2) inhibitors are a new class of antidiabetic drugs that exhibit multiple extraglycemic effects. However, there are conflicting results regarding the effects of SGLT2 inhibition on energy expenditure and thermogenesis. Therefore, we investigated the effect of ipragliflozin (a selective SGLT2 inhibitor) on energy metabolism.
Methods
Six-week-old male 129S6/Sv mice with a high propensity for adipose tissue browning were randomly assigned to three groups: normal chow control, 60% high-fat diet (HFD)-fed control, and 60% HFD-fed ipragliflozin-treated groups. The administration of diet and medication was continued for 16 weeks.
Results
The HFD-fed mice became obese and developed hepatic steatosis and adipose tissue hypertrophy, but their random glucose levels were within the normal ranges; these features are similar to the metabolic features of a prediabetic condition. Ipragliflozin treatment markedly attenuated HFD-induced hepatic steatosis and reduced the size of hypertrophied adipocytes to that of smaller adipocytes. In the ipragliflozin treatment group, uncoupling protein 1 (Ucp1) and other thermogenesis-related genes were significantly upregulated in the visceral and subcutaneous adipose tissue, and fatty acid oxidation was increased in the brown adipose tissue. These effects were associated with a significant reduction in the insulin-to-glucagon ratio and the activation of the AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1) pathway in the liver and adipose tissue.
Conclusion
SGLT2 inhibition by ipragliflozin showed beneficial metabolic effects in 129S6/Sv mice with HFD-induced obesity that mimics prediabetic conditions. Our data suggest that SGLT2 inhibitors, through their upregulation of energy expenditure, may have therapeutic potential in prediabetic obesity. -
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Reviews
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- Muthu Periasamy, Jose Luis Herrera, Felipe C. G. Reis
- Diabetes Metab J. 2017;41(5):327-336. Published online October 24, 2017
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Abstract
PDFPubReader ePub
Obesity and diabetes has become a major epidemic across the globe. Controlling obesity has been a challenge since this would require either increased physical activity or reduced caloric intake; both are difficult to enforce. There has been renewed interest in exploiting pathways such as uncoupling protein 1 (UCP1)-mediated uncoupling in brown adipose tissue (BAT) and white adipose tissue to increase energy expenditure to control weight gain. However, relying on UCP1-based thermogenesis alone may not be sufficient to control obesity in humans. On the other hand, skeletal muscle is the largest organ and a major contributor to basal metabolic rate and increasing energy expenditure in muscle through nonshivering thermogenic mechanisms, which can substantially affect whole body metabolism and weight gain. In this review we will describe the role of Sarcolipin-mediated uncoupling of Sarcoplasmic Reticulum Calcium ATPase (SERCA) as a potential mechanism for increased energy expenditure both during cold and diet-induced thermogenesis.
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- Masayuki Saito
- Diabetes Metab J. 2013;37(1):22-29. Published online February 15, 2013
- DOI: https://doi.org/10.4093/dmj.2013.37.1.22
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Abstract
PDFPubReader ePub
Brown adipose tissue (BAT) is recognized as the major site of sympathetically activated nonshivering thermogenesis during cold exposure and after spontaneous hyperphagia, thereby controling whole-body energy expenditure and body fat. In adult humans, BAT has long been believed to be absent or negligible, but recent studies using fluorodeoxyglucose-positron emission tomography, in combination with computed tomography, demonstrated the existence of metabolically active BAT in healthy adult humans. Human BAT is activated by acute cold exposure, being positively correlated to cold-induced increases in energy expenditure. The metabolic activity of BAT differs among individuals, being lower in older and obese individuals. Thus, BAT is recognized as a regulator of whole-body energy expenditure and body fat in humans as in small rodents, and a hopeful target combating obesity and related disorders. In fact, there are some food ingredients such as capsaicin and capsinoids, which have potential to activate and recruit BAT via activity on the specific receptor, transient receptor potential channels, thereby increasing energy expenditure and decreasing body fat modestly and consistently.
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