ArticleNutrition & metabolism2014
Miglitol increases energy expenditure by upregulating uncoupling protein 1 of brown adipose tissue and reduces obesity in dietary-induced obese mice.
Article in Nutrition & metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 26 citations in OpenAlex.
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- Hypothalamic PDE3B deficiency alters body weight and glucose homeostasis in mouseThe Journal of endocrinology · 2018Article
- Serum levels of uncoupling proteins in patients with differential insulin resistance: A community-based cohort study.Medicine · 2017Article
- Postprandial Increase in Energy Expenditure Correlates with Body Weight Reduction in Patients with Type 2 Diabetes Receiving Diet Therapy.Journal of atherosclerosis and thrombosis · 2017Article
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- Selection of Suitable Reference Genes for Quantitative Real-Time PCR Normalization in Three Types of Rat Adipose Tissue.International journal of molecular sciences · 2016Article
- Mice fed fish oil diet and upregulation of brown adipose tissue thermogenic markers.European journal of nutrition · 2016Article
- Review: Miglitol has potential as a therapeutic drug against obesity.Nutrition & metabolism · 2015Review
- A review on effects of conjugated linoleic fatty acid (CLA) upon body composition and energetic metabolism.Journal of the International Society of Sports Nutrition · 2015Review
- Crude extracts from Lycium barbarum suppress SREBP-1c expression and prevent diet-induced fatty liver through AMPK activation.BioMed research international · 2014Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMiglitol is an oral anti-diabetic drug that acts by inhibiting carbohydrate absorption in the small intestine. Recent studies have shown that miglitol reduces obesity in humans and rodents. However, its mechanisms have remained unclear. The purpose of this study was to determine whether miglitol generates heat by activating uncoupling protein 1 (UCP1), an enzyme involved in thermogenesis, in brown adipose tissue (BAT) in mice.
methodsFour-week-old male C57BL/6 J mice were fed a high-fat diet alone (HF) or a high fat diet plus miglitol (HFM). Oxygen consumption (VO2) was used to estimate metabolic rate. A thermal imaging camera was used to quantify heat generation from interscapular brown adipose tissue. We analyzed the protein and gene expressions of UCP1 and the expressions of four proteins related to β3-adrenergic signaling in the pathway activating UCP1 (protein kinase A (PKA), hormone-sensitive lipase (HSL), p38 α mitogen-activated protein kinase (p38αMAPK) and peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α)).
resultsAt 8 weeks, body weight, epididymal and subcutaneous white adipose tissue and the HOMA-R value of the HFM mice were significantly less than those of the HF mice. Food intake was not different between the HF and HFM mice. VO2 and BAT temperature were significantly higher in the HFM mice. Miglitol significantly enhanced the gene and protein expressions of UCP1 and the expressions of proteins related to β3-adrenergic signaling.
conclusionsMiglitol's anti-obesity effect was attributed to increased energy expenditure by upregulating UCP1 in BAT (i.e., by thermogenesis) and to enhancement of β3-adrenergic signaling in BAT.
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Registered trials
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