Brain-derived neurotrophic factor in VMH as the causal factor for and therapeutic tool to treat visceral adiposity and hyperleptinemia in type 2 diabetic Goto–Kakizaki rats
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We previously reported that the type 2 diabetic Goto-Kakizaki (GK) rats at young adult ages (6-12 weeks) exhibited increased visceral fat mass and hyperleptinemia, due to hyperphagia caused primarily by neuropeptide Y (NPY) overexpression in the hypothalamic arcuate nucleus. Later, we found that GK rats continued to exhibit mesenteric fat accumulation and hyperleptinemia at least until 26 weeks of age, while hyperphagia and NPY overexpression ceased at 15 weeks of age. Therefore, we hypothesized that the long-lasting fat accumulation and hyperleptinemia are due to unidentified brain dysfunction other than NPY overexpression. In GK rats aged 26 weeks, glucose transporter-2 (GLUT2) mRNA expression in ventromedial hypothalamus (VMH) was markedly reduced in parallel with significant decreases in brain-derived neurotrophic factor (BDNF) mRNA level and BDNF-expressing cell numbers in the VMH. Pharmacologic inhibition of glucose utilization reduced BDNF mRNA expression in VMH in vivo and in vitro. The results suggested that impaired glucose utilization caused the reduction of BDNF. On the other hand, intracerebroventricular injection of BDNF for 6 days ameliorated hyperleptinemia in a long-lasting manner concurrently with feeding suppression in GK rats. Restricted feeding paired to BDNF-treated rats reduced plasma leptin level only transiently. BDNF treatment also reduced mesenteric fat mass in GK rats. These results reveal a novel action mode of BDNF to long-lastingly counteract visceral adiposity and hyperleptinemia in addition to and independently of its anorexigenic action. These results suggest that visceral fat accumulation and hyperleptinemia are at least partly due to the reduction of BDNF in VMH primarily caused by impaired glucose utilization in GK rats. The BDNF supplementation could provide an effective treatment of visceral obesity, hyperleptinemia and leptin resistance in type 2 diabetes.
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Injection of BDNF into the VMH increases the metabolic rate and reduces visceral adiposity.
“Conversely, injection of BDNF into the VMH was observed to increase the metabolic rate and reduce visceral adiposity [49, 50]”
From High-intensity interval training or lactate administration combined with aerobic training enhances visceral fat loss while promoting VMH neuroplasticity in female rats (2024) · cites this paper as [50]
The Methods section (page unavailable) says BDNF was injected intracerebroventricularly, not into the VMH. The Results section reports reduced mesenteric fat in BDNF-treated GK rats, while the Introduction describes increased energy expenditure after intracerebroventricular BDNF injection in earlier work. The paper therefore supports the adiposity finding and discusses the metabolic effect, but not the claimed VMH injection or a measured increase in metabolic rate from that injection. (LLM, conf=0.86)
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- Authors
- Maekawa, F., Fujiwara, K., Toriya, M., Maejima, Y., Nishio, T., Toyoda, Y., Nohara, K., Yashiro, T., & Yada, T.
- Affiliations
- Jichi Medical University (JP)
- Meijo University (JP)
- National Institute for Environmental Studies (JP)
- Corresponding author
- Yada, Toshihiko
- ORCID
- Venue
- Frontiers in Synaptic Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2013
- Volume
- 5
- Pages
- 7-7
- ISSN
- 1663-3563 (ISSN-L)
- PMC
- PMC3788348
- OpenAlex
- W2080089519
- Cited by
- 19
- References
- 54
- Citations by year
- 2026: 1 · 2024: 1 · 2022: 3 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 3
- FWCI
- 0.90
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Synaptic Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Kowa Company
- Ministry of Education, Culture, Sports, Science and Technology (2011-2015, 23310043, 10036069, 23390044, 2013−2017)
- Dainippon Sumitomo Pharma
- Kowa Life Science Foundation
- Japan Diabetes Foundation
- Japan Society for the Promotion of Science (23390044, 23310043, 24790199, 24659101, 24590307, 23126523, 24591341)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- brain-derived neurotrophic factor, ventromedial hypothalamus, visceral fat, hyperleptinemia, leptin resistance, type 2 diabetes, Goto-Kakizaki rats, mesenteric fat, GLUT2, glucose utilization, neuropeptide Y, hyperphagia, intracerebroventricular administration, feeding inhibition, obesity treatment
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