ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Intraflagellar-transport A dysfunction causes hyperphagia-induced systemic insulin resistance in a pre-obese state.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 4 citations in OpenAlex.
- Primary Cilia as Integrative Hubs of Metabolic Signaling in Type 2 Diabetes: Inter-Organ Evidence From Central, Peripheral, and Pancreatic Islet Tissues.Journal of cellular physiology · 2026Review
- Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026Review
- Genetic interaction ofbioRxiv : the preprint server for biology · 2025Article
- IFT139 regulates Hedgehog signaling and cilia structure through ciliary protein localization.Biology open · 2025Article
- Mitochondria-associated membranes contribution to exercise-mediated alleviation of hepatic insulin resistance: Contrasting high-intensity interval training with moderate-intensity continuous training in a high-fat diet mouse model.Journal of diabetes · 2024Article
- Intraflagellar Transport Proteins as Regulators of Primary Cilia Length.Frontiers in cell and developmental biology · 2021Review
- MetAP2 inhibition reduces food intake and body weight in a ciliopathy mouse model of obesity.JCI insight · 2020Article
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Authors and funding
10 authors at 1 institution in 1 country.
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Abstract
Deletion of murine Thm1, an intraflagellar transport A (IFT-A) component that mediates ciliary protein trafficking, causes hyperphagia, obesity, and metabolic syndrome. The role of Thm1 or IFT-A in adipogenesis and insulin sensitivity is unknown. Here, we report that Thm1 knockdown in 3T3-L1 pre-adipocytes promotes adipogenesis and enhances insulin sensitivity in vitro. Yet, pre-obese Thm1 conditional knockout mice show systemic insulin resistance. While insulin-induced AKT activation in Thm1 mutant adipose depots and skeletal muscle are similar to those of control littermates, an attenuated insulin response arises in the mutant liver. Insulin treatment of control and Thm1 mutant primary hepatocytes results in similar AKT activation. Moreover, pair-feeding Thm1 conditional knockout mice produces a normal insulin response, both in the liver and systemically. Thus, hyperphagia caused by a cilia defect, induces hepatic insulin resistance via a non-cell autonomous mechanism. In turn, hepatic insulin resistance drives systemic insulin resistance prior to an obese phenotype. These data demonstrate that insulin signaling across cell types is regulated differentially, and that the liver is particularly susceptible to hyperphagia-induced insulin resistance and a critical determinant of systemic insulin resistance.
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