{"id":333,"title":"Testosterone treatment prevents most gonadectomy-induced metabolic and skeletal deficiencies in female mice","title_zh":"睾酮治疗可预防去卵巢雌鼠多数代谢与骨骼缺陷","url":"https://pubmed.ncbi.nlm.nih.gov/42964108","doi":"10.3389/fendo.2026.1940100","pmid":"42964108","journal":"Front Endocrinol (Lausanne)","kind":"paper","lang":"en","published_at":"2026-10-16T00:00:00+00:00","fetched_at":"2026-11-08T03:44:05+00:00","authors":["Kruger RE","Yohannes H","Cho E","Eisner L","Pfau DR","Chan-Sui RK","Migotsky N","Monteiro da Rocha A","Killian ML","Moravek MB","Padmanabhan V","Shikanov A"],"primary_topic":"repro-endo","topics":[{"slug":"repro-endo","score":2.0,"hits":["menopause","primary ovarian insufficiency"]},{"slug":"oocyte","score":1.0,"hits":["ovarian"]},{"slug":"fertility-preservation","score":1.0,"hits":["gonadotoxic"]},{"slug":"repro-tox","score":1.0,"hits":["gonadotoxic"]}],"topic_score":2.0,"preference_score":0.0,"preference_labels":[],"llm_score":63.0,"final_score":63.0,"score_dims":{"novelty":66,"rigor":72,"impact":60,"relevance":55,"translation":55},"recommend_reason":"选题涉及卵巢激素缺失后的代谢与骨骼结局，对生殖内分泌和绝经/卵巢功能不全管理有参考价值；但为小样本小鼠实验，离ART临床决策较远，适合浏览而非必读。","keywords":["睾酮","去卵巢","卵巢激素缺失","代谢稳态","骨密度","小鼠模型"],"selected":1,"story_id":391,"llm_provider":"deepseek","llm_model":"deepseek-flash","llm_effort":"low","source_key":"pubmed-endo-genetics","source_name":"PubMed · 生殖内分泌/遗传/保存","source_tier":1,"mention_count":1,"has_interpretation":false,"journal_key":"front-endo","journal_tier":"standard","journal_if":3.9,"is_mock":false,"summary_zh":"研究以8周龄CD-1雌鼠为对象，行假手术或去卵巢，并皮下植入含10 mg睾酮或空胶囊，分为四组（每组n=7–8），处理6周。结果显示，睾酮可缓解去卵巢引起的高血糖和糖耐量受损，但未能预防血脂异常和脂肪细胞肥大；无论卵巢状态如何，睾酮还升高循环甘油三酯、心脏重量、股骨小梁骨密度和桡向强度。结论提示睾酮仅补偿卵巢激素丢失的部分代谢与骨骼后果，雄激素与雌激素在代谢稳态中作用不同，或为卵巢功能不全、绝经及雄激素相关治疗管理提供参考。","summary":"Ovarian hormone depletion, whether due to ovariectomy, primary ovarian insufficiency, menopause, or gonadotoxic therapies, is associated with metabolic and skeletal dysfunction, while hyperandrogenic states such as polyendocrine metabolic ovarian syndrome are also linked to increased cardiometabolic risk. However, whether testosterone exacerbates, mitigates, or modifies the consequences of ovarian hormone loss remains poorly understood. This study examined whether testosterone treatment ameliorates ovariectomy-induced metabolic and skeletal impairments using an adult female mouse model. Eight-week-old CD-1 mice underwent sham surgery or ovariectomy and were implanted subcutaneously with capsules containing 10 mg testosterone or empty control capsules, yielding four experimental groups: Blank+Intact (n=7), Blank+OVX (n=7), Testosterone+Intact (n=7), and Testosterone+OVX (n=8). Each treatment combination resulted in hormonal milieus distinct to each group. After six weeks of treatment, testosterone mitigated ovariectomy-induced hyperglycemia and impaired glucose tolerance but did not prevent dyslipidemia or adipocyte hypertrophy (two-way ANOVA with Tukey's post hoc test, p<0.05). Testosterone treatment also increased circulating triglycerides, heart weight, femoral trabecular bone density, and radial strength independent of ovarian status. These findings indicate that testosterone compensates for some, but not all, metabolic and skeletal consequences of ovarian hormone loss, revealing distinct roles for androgens and estrogens in metabolic homeostasis. This may inform clinical management of ovarian insufficiency, menopause, hyperandrogenic disorders, and testosterone-based therapies.","interpretation_basis":null,"fulltext_status":null,"interpretation":null,"fulltext":{"available":false,"status":null,"reason":"尚未抓取全文（未入选、分数未达阈值，或还没跑 fulltext 步骤）","pmcid":null,"license":null,"chars":0,"source":null,"fetched_at":null}}