ArticleScientific reports2018
Endogenous calcitonin regulates lipid and glucose metabolism in diet-induced obesity mice.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 27 citations in OpenAlex.
- Prenatal nutrition supplementation and growth biomarkers in preadolescent Bangladeshi children: A birth cohort study.Maternal & child nutrition · 2022Trial
- [Liver-bone axis: novel mechanisms and strategies for MAFLD regulation].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Article
- The roles of hepatokine and osteokine in liver-bone crosstalk: Advance in basic and clinical aspects.Frontiers in endocrinology · 2023Review
- Mediators of Amylin Action in Metabolic Control.Journal of clinical medicine · 2022Review
- N-linoleyltyrosine ameliorates high-fat diet-induced obesity in C57BL/6 miceFrontiers in endocrinology · 2022Article
- Mono and dual agonists of the amylin, calcitonin, and CGRP receptors and their potential in metabolic diseases.Molecular metabolism · 2021Review
- Article
- An Analysis of the Anti-Neuropathic Effects of Qi She Pill Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2020Article
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcitonin (CT) plays an important role in calcium homeostasis, and its precursor, proCT, is positively associated with the body mass index in the general human population. However, the physiological role of endogenous CT in the regulation of metabolism remains unclear. Knockout mice with gene-targeted deletion of exon 4 of Calca (CT KO) were generated by targeted modification in embryonic stem cells. Male mice were used in all experiments and were fed a slightly higher fat diet than the standard diet. The CT KO mice did not exhibit any abnormal findings in appearance, but exhibited weight loss from 15 months old, i.e., significantly decreased liver, adipose tissue, and kidney weights, compared with wild-type control mice. Furthermore, CT KO mice exhibited significantly decreased fat contents in the liver, lipid droplets in adipose tissues, serum glucose, and lipid levels, and significantly increased insulin sensitivity and serum adiponectin levels. CT significantly promoted 3T3-L1 adipocyte differentiation and suppressed adiponectin release. These results suggested that CT gene deletion prevents obesity, hyperglycemia, and hyperlipidemia in aged male mice. This is the first definitive evidence that CT may contribute to glucose and lipid metabolism in aged male mice, possibly via decreased adiponectin secretion from adipocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.