ArticleBiochimica et biophysica acta. Molecular basis of disease2017
Germline deletion of Krüppel-like factor 14 does not increase risk of diet induced metabolic syndrome in male C57BL/6 mice.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Adipocyte-specific Krüppel-like factor 14 overexpression confers sex-biased protection from weight gain on a high-fat diet.Physiological reports · 2025Article
- The Role of APOA-I in Alzheimer's Disease: Bridging Peripheral Tissues and the Central Nervous System.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Article
- APOE and KLF14 genetic variants are sex-specific for low high-density lipoprotein cholesterol identified by a genome-wide association study.Genetics and molecular biology · 2022Article
- Murine deficiency of peroxisomal L-bifunctional protein (EHHADH) causes medium-chain 3-hydroxydicarboxylic aciduria and perturbs hepatic cholesterol homeostasis.Cellular and molecular life sciences : CMLS · 2021Article
- Deletion of Trim28 in committed adipocytes promotes obesity but preserves glucose tolerance.Nature communications · 2021Article
- DNA methylation microarrays identify epigenetically regulated lipid related genes in obese patients with hypercholesterolemia.Molecular medicine (Cambridge, Mass.) · 2020Article
- Dietary supplement of Yunkang 10 green tea and treadmill exercise ameliorate high fat diet induced metabolic syndrome of C57BL/6 J mice.Nutrition & metabolism · 2020Article
- Transcription Factor KLF14 and Metabolic Syndrome.Frontiers in cardiovascular medicine · 2020Review
- Overexpression of KLF14 protects against immune-mediated hepatic injury in mice.Laboratory investigation; a journal of technical methods and pathology · 2019Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe transcription factor Krüppel-like factor 14 (KLF14) has been associated with type 2 diabetes and high-density lipoprotein-cholesterol (HDL-C) through genome-wide association studies. The mechanistic underpinnings of KLF14's control of metabolic processes remain largely unknown. We studied the physiological roles of KLF14 in a knockout (KO) mouse model.
methodsMale whole body Klf14 KO mice were fed a chow or high fat diet (HFD) and diet induced phenotypes were analyzed. Additionally, tissue-specific expression of Klf14 was determined using RT-PCR, RNA sequencing, immunoblotting and whole mount lacZ staining. Finally, the consequences of KLF14 loss-of-function were studied using RNA sequencing in tissues with relatively high Klf14 expression levels.
resultsKLF14 loss-of-function did not affect HFD-induced weight gain or insulin resistance. Fasting plasma concentrations of glucose, insulin, cholesterol, HDL-C and ApoA-I were also comparable between Klf14
conclusionsWhole body loss of KLF14 function in male mice does not result in metabolic abnormalities as assessed under chow and HFD conditions. Mostly likely there is redundancy for the role of KLF14 in the mouse and a diverging function in humans.
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