ArticlePflugers Archiv : European journal of physiology2018
Telmisartan prevents diet-induced obesity and preserves leptin transport across the blood-brain barrier in high-fat diet-fed mice.
Article in Pflugers Archiv : European journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 30 citations in OpenAlex.
- Serum S100β and neuron-specific enolase correlate with obesity parameters in Mexican children.International journal of obesity (2005) · 2026Article
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- Increase in body weight is lowered when mice received fecal microbiota transfer from donor mice treated with the ATFrontiers in pharmacology · 2024Article
- The Mechanism of Leptin Resistance in Obesity and Therapeutic Perspective.Advances in experimental medicine and biology · 2024Review
- Addressing Peroxisome Proliferator-Activated Receptor-gamma in 3-Nitropropionic Acid-Induced Striatal Neurotoxicity in Rats.Molecular neurobiology · 2022Article
- Article
- The AT1 Receptor Blocker Telmisartan Reduces Intestinal Mucus Thickness in Obese Mice.Frontiers in pharmacology · 2022Article
- Telmisartan prevents high-fat diet-induced neurovascular impairments and reduces anxiety-like behavior.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Characterization of ACE Inhibitors and ATLife (Basel, Switzerland) · 2021Article
- Impaired Leptin Signalling in Obesity: Is Leptin a New Thermolipokine?International journal of molecular sciences · 2021Review
- Effect of High-Fat Diets on Oxidative Stress, Cellular Inflammatory Response and Cognitive Function.Nutrients · 2019 · on this mapReview
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Authors and funding
8 authors at 5 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Obesity is a global health problem and treatment options are still insufficient. When chronically treated with the angiotensin II receptor blocker telmisartan (TEL), rodents do not develop diet-induced obesity (DIO). However, the underlying mechanism for this is still unclear. Here we investigated whether TEL prevents leptin resistance by enhancing leptin uptake across the blood-brain barrier (BBB). To address this question, we fed C57BL/6 mice a high-fat diet (HFD) and treated them daily with TEL by oral gavage. In addition to broadly characterizing the metabolism of leptin, we determined leptin uptake into the brain by measuring BBB transport of radioactively labeled leptin after long-term and short-term TEL treatment. Additionally, we assessed BBB integrity in response to angiotensin II in vitro and in vivo. We found that HFD markedly increased body weight, energy intake, and leptin concentration but that this effect was abolished under TEL treatment. Furthermore, glucose control and, most importantly, leptin uptake across the BBB were impaired in mice on HFD, but, again, both were preserved under TEL treatment. BBB integrity was not impaired due to angiotensin II or blocking of angiotensin II receptors. However, TEL did not exhibit an acute effect on leptin uptake across the BBB. Our results confirm that TEL prevents DIO and show that TEL preserves leptin transport and thereby prevents leptin resistance. We conclude that the preservation of leptin sensitivity is, however, more a consequence than the cause of TEL preventing body weight gain.
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