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1.
Int J Mol Sci ; 24(10)2023 May 10.
Article in English | MEDLINE | ID: mdl-37239868

ABSTRACT

Insulin resistance is one of the main characteristics of metabolic syndrome (MetS) and the main cause of the development of type II diabetes. The high prevalence of this syndrome in recent decades has made it necessary to search for preventive and therapeutic agents, ideally of natural origin, with fewer side effects than conventional pharmacological treatments. Tea is widely known for its medicinal properties, including beneficial effects on weight management and insulin resistance. The aim of this study was to analyze whether a standardized extract of green and black tea (ADM® Complex Tea Extract (CTE)) prevents the development of insulin resistance in mice with MetS. For this purpose, C57BL6/J mice were fed for 20 weeks with a standard diet (Chow), a diet with 56% kcal from fat and sugar (HFHS) or an HFHS diet supplemented with 1.6% CTE. CTE supplementation reduced body weight gain, adiposity and circulating leptin levels. Likewise, CTE also exerted lipolytic and antiadipogenic effects in 3T3-L1 adipocyte cultures and in the C. elegans model. Regarding insulin resistance, CTE supplementation significantly increased plasma adiponectin concentrations and reduced the circulating levels of insulin and the HOMA-IR. Incubation of liver, gastrocnemius muscle and retroperitoneal adipose tissue explants with insulin increased the pAkt/Akt ratio in mice fed with Chow and HFHS + CTE but not in those fed only with HFHS. The greater activation of the PI3K/Akt pathway in response to insulin in mice supplemented with CTE was associated with a decrease in the expression of the proinflammatory markers Mcp-1, IL-6, IL-1ß or Tnf-α and with an overexpression of the antioxidant enzymes Sod-1, Gpx-3, Ho-1 and Gsr in these tissues. Moreover, in skeletal muscle, mice treated with CTE showed increased mRNA levels of the aryl hydrocarbon receptor (Ahr), Arnt and Nrf2, suggesting that the CTE's insulin-sensitizing effects could be the result of the activation of this pathway. In conclusion, supplementation with the standardized extract of green and black tea CTE reduces body weight gain, exerts lipolytic and antiadipogenic effects and reduces insulin resistance in mice with MetS through its anti-inflammatory and antioxidant effects.


Subject(s)
Camellia sinensis , Diabetes Mellitus, Type 2 , Insulin Resistance , Metabolic Syndrome , Mice , Animals , Metabolic Syndrome/drug therapy , Metabolic Syndrome/complications , Tea , Diabetes Mellitus, Type 2/drug therapy , Phosphatidylinositol 3-Kinases , Caenorhabditis elegans , Proto-Oncogene Proteins c-akt , Plant Extracts/pharmacology , Plant Extracts/therapeutic use , Obesity/metabolism , Weight Gain , Insulin , Antioxidants/pharmacology , Antioxidants/therapeutic use , Dietary Supplements , Diet, High-Fat/adverse effects , Mice, Inbred C57BL
2.
Nutrients ; 12(2)2020 Feb 14.
Article in English | MEDLINE | ID: mdl-32075050

ABSTRACT

BACKGROUND: We previously described a novel micronutrient blend that behaves like a putative calorie restriction mimetic. The aim of this paper was to analyze the beneficial effects of our micronutrient blend in mice and C. elegans, and compare them with calorie restriction. METHODS: Whole transcriptomic analysis was performed in the brain cortex, skeletal muscle and heart in three groups of mice: old controls (30 months), old + calorie restriction and old + novel micronutrient blend. Longevity and vitality were tested in C. elegans. RESULTS: The micronutrient blend elicited transcriptomic changes in a manner similar to those in the calorie-restricted group and different from those in the control group. Subgroup analysis revealed that nuclear hormone receptor, proteasome complex and angiotensinogen genes, all of which are known to be directly related to aging, were the most affected. Furthermore, a functional analysis in C. elegans was used. We found that feeding C. elegans the micronutrient blend increased longevity as well as vitality. CONCLUSIONS: We describe a micronutrient supplement that causes similar changes (transcriptomic and promoting longevity and vitality) as a calorie restriction in mice and C. elegans, respectively, but further studies are required to confirm these effects in humans.


Subject(s)
Animal Nutritional Physiological Phenomena , Caenorhabditis elegans/genetics , Caenorhabditis elegans/physiology , Caloric Restriction , Eating/genetics , Eating/physiology , Exome Sequencing/methods , Locomotion/genetics , Longevity/genetics , Mice/genetics , Mice/physiology , Micronutrients/administration & dosage , Transcriptome/genetics , Animals , Humans
3.
Int J Med Sci ; 14(5): 444-451, 2017.
Article in English | MEDLINE | ID: mdl-28539820

ABSTRACT

Aims.Bifidobacterium pseudocatenulatum CECT 7765 improves metabolic and immunological altered functions in high fat fed mice, however little is known about the effects of potential probiotics on vascular reactivity. The aim of the present study was to investigate the effects of a potential probiotic strain, Bifidobacterium pseudocatenulatum CECT 7765, on vascular response in obese mice. Methods. Aorta samples were obtained from mice, which were divided into three groups: a control group, receiving a standard diet; an obese group, receiving a high-fat diet; and an obese group receiving high-fat diet and a daily dose of B. pseudocatenulatum CECT 7765 by oral gavage. Aortic rings were suspended in organ baths for isometric recording of tension. mRNA expression of eNOS was evaluated by real-time polymerase chain reaction. Results. Contractions induced by KCl, noradrenaline and thromboxane analogue were 33%, 30% and 45% lower respectively in aortic rings from obese mice. Bifidobacteria administration reversed this effect. eNOS inhibition increased the response to noradrenaline in the three groups with a significant lower magnitude in aortic rings from obese mice receiving bifidobacteria supplement. Acetylcholine caused a greater vasodilation in aorta from obese group (46±3% for control and 69±4% for obese group; p<0.05) and bifidobacteria reversed it (57±5%). Response to sodium nitroprusside was displaced 2.9 times to the left in a parallel manner in obese group. Relaxation to sodium nitroprusside remained unchanged in the bifidobacteria fed group. There was about five-fold decreased mRNA expression of eNOS in aortic segments from the group receiving bifidobacteria. Conclusion.Bifidobacterium pseudocatenulatum CECT 7765 restores the obesity-induced altered vascular function mainly by reducing nitric oxide release.


Subject(s)
Bifidobacterium pseudocatenulatum/chemistry , Nitric Oxide Synthase Type III/genetics , Obesity/diet therapy , Probiotics/administration & dosage , Animals , Diet, High-Fat/adverse effects , Dietary Supplements , Gene Expression Regulation/drug effects , Humans , Mice , Mice, Obese , Nitric Oxide/metabolism , Nitroprusside/administration & dosage , Obesity/genetics , Obesity/pathology , Probiotics/chemistry , Vascular Remodeling/drug effects
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