Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant Mice

To explore the hydroxy-alpha-sanshool (HAS) effects on the intestinal metabolites of insulin-resistant mice, the blank group (BG), model group (MG), and HAS dose group (DG) were designed. The insulin resistance (IR) model was induced through streptozotocin (STZ) combined with a high-fat and high-sug...

Full description

Bibliographic Details
Main Authors: Fangyan Xu, Yuping Zhu, Mintao Lu, Likang Qin, Degang Zhao, Tingyuan Ren
Format: Article
Language:English
Published: MDPI AG 2022-07-01
Series:Foods
Subjects:
Online Access:https://www.mdpi.com/2304-8158/11/14/2040
_version_ 1797406419348094976
author Fangyan Xu
Yuping Zhu
Mintao Lu
Likang Qin
Degang Zhao
Tingyuan Ren
author_facet Fangyan Xu
Yuping Zhu
Mintao Lu
Likang Qin
Degang Zhao
Tingyuan Ren
author_sort Fangyan Xu
collection DOAJ
description To explore the hydroxy-alpha-sanshool (HAS) effects on the intestinal metabolites of insulin-resistant mice, the blank group (BG), model group (MG), and HAS dose group (DG) were designed. The insulin resistance (IR) model was induced through streptozotocin (STZ) combined with a high-fat and high-sugar diet. Based on the availability of the model, the HAS dose was given by gavage for 28 days. The determination of cecum and key serum indexes was made, including the contents of insulin (INS), triglycerides (TG), total cholesterol (TC), glycosylated serum protein (GSP), and glycosylated hemoglobin (GHb). The changes in gut microbiota and metabolites in cecal contents were detected by 16S rRNA gene amplicon sequencing and UPLC/HRMS technology, respectively. The results that the levels of GSP, GHb, TG, and TC were significantly increased; this was not the case for INS; or for the changes in the gut microbiota and metabolites in MG. However, the intervention of HAS effectively reversed these changes, for instance, it decreased levels of GSP, GHb, TG, TC, and alterations of metabolite composition for linoleic acid and tyrosine metabolism and recovered trends of declining species diversity and richness of the gut microbiota in MG. It was indicated that HAS alleviated IR by regulating the gut microbiota and metabolites and affecting lipid and amino acid metabolism pathways.
first_indexed 2024-03-09T03:26:10Z
format Article
id doaj.art-27633cba8fa4459794cdcca1331935ce
institution Directory Open Access Journal
issn 2304-8158
language English
last_indexed 2024-03-09T03:26:10Z
publishDate 2022-07-01
publisher MDPI AG
record_format Article
series Foods
spelling doaj.art-27633cba8fa4459794cdcca1331935ce2023-12-03T15:02:34ZengMDPI AGFoods2304-81582022-07-011114204010.3390/foods11142040Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant MiceFangyan Xu0Yuping Zhu1Mintao Lu2Likang Qin3Degang Zhao4Tingyuan Ren5College of Brewing and Food Engineering, Guizhou University, Guiyang 550025, ChinaSchool of Basic Medicine, Guizhou Medical University, Guiyang 550025, ChinaCollege of Brewing and Food Engineering, Guizhou University, Guiyang 550025, ChinaCollege of Brewing and Food Engineering, Guizhou University, Guiyang 550025, ChinaCollege of Brewing and Food Engineering, Guizhou University, Guiyang 550025, ChinaCollege of Brewing and Food Engineering, Guizhou University, Guiyang 550025, ChinaTo explore the hydroxy-alpha-sanshool (HAS) effects on the intestinal metabolites of insulin-resistant mice, the blank group (BG), model group (MG), and HAS dose group (DG) were designed. The insulin resistance (IR) model was induced through streptozotocin (STZ) combined with a high-fat and high-sugar diet. Based on the availability of the model, the HAS dose was given by gavage for 28 days. The determination of cecum and key serum indexes was made, including the contents of insulin (INS), triglycerides (TG), total cholesterol (TC), glycosylated serum protein (GSP), and glycosylated hemoglobin (GHb). The changes in gut microbiota and metabolites in cecal contents were detected by 16S rRNA gene amplicon sequencing and UPLC/HRMS technology, respectively. The results that the levels of GSP, GHb, TG, and TC were significantly increased; this was not the case for INS; or for the changes in the gut microbiota and metabolites in MG. However, the intervention of HAS effectively reversed these changes, for instance, it decreased levels of GSP, GHb, TG, TC, and alterations of metabolite composition for linoleic acid and tyrosine metabolism and recovered trends of declining species diversity and richness of the gut microbiota in MG. It was indicated that HAS alleviated IR by regulating the gut microbiota and metabolites and affecting lipid and amino acid metabolism pathways.https://www.mdpi.com/2304-8158/11/14/2040hydroxy-alpha-sanshoolinsulin resistantmetabolismintestines
spellingShingle Fangyan Xu
Yuping Zhu
Mintao Lu
Likang Qin
Degang Zhao
Tingyuan Ren
Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant Mice
Foods
hydroxy-alpha-sanshool
insulin resistant
metabolism
intestines
title Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant Mice
title_full Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant Mice
title_fullStr Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant Mice
title_full_unstemmed Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant Mice
title_short Effects of Hydroxy-Alpha-Sanshool on Intestinal Metabolism in Insulin-Resistant Mice
title_sort effects of hydroxy alpha sanshool on intestinal metabolism in insulin resistant mice
topic hydroxy-alpha-sanshool
insulin resistant
metabolism
intestines
url https://www.mdpi.com/2304-8158/11/14/2040
work_keys_str_mv AT fangyanxu effectsofhydroxyalphasanshoolonintestinalmetabolismininsulinresistantmice
AT yupingzhu effectsofhydroxyalphasanshoolonintestinalmetabolismininsulinresistantmice
AT mintaolu effectsofhydroxyalphasanshoolonintestinalmetabolismininsulinresistantmice
AT likangqin effectsofhydroxyalphasanshoolonintestinalmetabolismininsulinresistantmice
AT degangzhao effectsofhydroxyalphasanshoolonintestinalmetabolismininsulinresistantmice
AT tingyuanren effectsofhydroxyalphasanshoolonintestinalmetabolismininsulinresistantmice