PMID- 37581324
OWN - NLM
STAT- Publisher
LR  - 20231220
IS  - 1873-4316 (Electronic)
IS  - 1389-2010 (Linking)
DP  - 2023 Aug 11
TI  - Salvia officinalis Improves Glycemia and Suppresses Pro-inflammatory Features in 
      Obese Rats with Metabolic Syndrome.
LID - 10.2174/1389201024666230811104740 [doi]
AB  - OBJECTIVES: Obesity is regarded as the main cause of metabolic diseases and a 
      core factor for all-cause mortality in the general population, notably from 
      cardiovascular disease. The majority of people with type 2 diabetes have obesity 
      and insulin resistance. Some evidence indicates that an individual with obesity 
      is approximately 10 times more likely to develop type 2 diabetes than someone 
      with moderate body weight. One of the most significant therapeutic herbs, Salvia 
      officinalis (Lamiaceae) (SAGE), possesses potent medicinal importance. The aim of 
      this article was to evaluate the anti-diabetic and antiobesity activity of SAGEAE 
      against HFD-induced obesity in rats. METHODS: : Thirty adult albino rats were 
      randomly divided into five equal groups: control, High-fat Diet (HFD) 
      administrated rats, HFD + Salvia officinalis Aqueous Extract (SAGEAE) (150 
      mg/kg.bw.), HFD + SAGEAE (300 mg/kg.bw.) and HFD + metformin (500 mg/kg.bw.). 
      Body weight, plasma biochemical parameters, oxidative stress, inflammatory 
      indicators, hepatic Phosphoenolpyruvate Carboxykinase 1 (PCK1), Glucokinase (GK), 
      brain Leptin Receptor (LepRb), Glucose Transporter-4 (GLUT4), Sirtuin 1 (SIRT1) 
      and mRNA33-5P gene signalling mRNA levels were all assessed after 8 weeks. A 
      histological examination of the liver was also performed to check for lipid 
      accumulation RESULTS: The administration of HFD resulted in increased body 
      weight, glucose, insulin, leptin, Total Cholesterol (TC), Triglycerides (TG), 
      Thiobarbaturic Acid Reactive Substances (TBARS), Monocyte Chemoattractant 
      Protein-1 (MCP1), Interleukine-6 (IL-6) and tumor necrosis factor-alpha (TNF- alpha) as 
      well as hepatic PCK1, brain LepRb and adipose tissue mRNA33-5P gene expression. 
      However, our findings revealed a significant reduction in adiponectin, 
      High-density Lipoproteincholesterol (HDL-C), reduced glutathione (GSH) and 
      Superoxide Dismutase (SOD) levels as well as the expression of hepatic GK and 
      adipose tissue SIRT1 and GLUT4 genes. Also, administration of SAGEAE 
      significantly normalized body weight, glucose, insulin, leptin, adiponectin, TC, 
      TG, HDL-C, TBARs, SOD, IL-6, MCP-1 and TNF-alpha in plasma and liver tissue of 
      HFD-treated rats. On the other hand, PCK1, GK, LepRb, SIRT1, GLUT4 and mRNA33-5P 
      gene expression was enhanced in obese rats when administrated with SAGEAE. 
      Histological and US studies support the biochemical, PCR and electrophoretic 
      results. CONCLUSION: The findings imply that SAGEAE could be used as a new 
      pharmaceutical formula in the treatment of obesity.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Alsherif, Diana A
AU  - Alsherif DA
AD  - Department of Radiology and Medical Imaging, Faculty of Applied Health Science 
      Technology, October 6th University, October 6th City, Egypt
FAU - Hussein, Mohammed A
AU  - Hussein MA
AUID- ORCID: 0000-0002-1811-2794
AD  - Department of Biotechnology, Faculty of Applied Health Science Technology, 
      October 6th University, October 6th City, Egypt
FAU - Abuelkasem, Suzan S
AU  - Abuelkasem SS
AD  - Department of Biochemistry, Faculty of Applied Health Science Technology, October 
      6th University, October 6th City, Egypt;
LA  - eng
PT  - Journal Article
DEP - 20230811
PL  - Netherlands
TA  - Curr Pharm Biotechnol
JT  - Current pharmaceutical biotechnology
JID - 100960530
SB  - IM
OTO - NOTNLM
OT  - GK
OT  - GLUT4 and mRNA33-5P
OT  - LepRb
OT  - PCK1
OT  - SAGE
OT  - SIRT2
OT  - adiponectin
OT  - insulin
OT  - leptin
EDAT- 2023/08/15 12:42
MHDA- 2023/08/15 12:42
CRDT- 2023/08/15 07:03
PHST- 2022/12/28 00:00 [received]
PHST- 2023/06/12 00:00 [revised]
PHST- 2023/06/26 00:00 [accepted]
PHST- 2023/08/15 12:42 [medline]
PHST- 2023/08/15 12:42 [pubmed]
PHST- 2023/08/15 07:03 [entrez]
AID - CPB-EPUB-133556 [pii]
AID - 10.2174/1389201024666230811104740 [doi]
PST - aheadofprint
SO  - Curr Pharm Biotechnol. 2023 Aug 11. doi: 10.2174/1389201024666230811104740.