Omega-3 PUFA and probiotics as a single formulation for insulin resistance and obesity: Evidence from animals to randomized clinical studies

Author(s):  
Nazarii Kobyliak ◽  
Tetyana Falalyeyeva ◽  
Galyna Mykhalchyshyn ◽  
Olexiy Savchuk ◽  
Dmytro Kyriienko ◽  
...  
Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1066
Author(s):  
Daniel González-Hedström ◽  
María de la Fuente-Fernández ◽  
Teresa Priego ◽  
Ana Isabel Martín ◽  
Sara Amor ◽  
...  

Olive-derived products, such as virgin olive oil (EVOO) and/or olive leaf extracts (OLE), exert anti-inflammatory, insulin-sensitizing and antihypertensive properties and may be useful for stabilizing omega 3 fatty acids (n-3 PUFA) due to their high content in antioxidant compounds. In this study, the addition of OLE 4:0.15 (w/w) to a mixture of algae oil (AO) rich in n-3 PUFA and EVOO (25:75, w/w) prevents peroxides formation after 12 months of storage at 30 °C. Furthermore, the treatment with the oil mixture (2.5 mL/Kg) and OLE (100 mg/Kg) for 24 month old Wistar rats in 21 days improved the lipid profile, increased the HOMA-IR and decreased the serum levels of miRNAs 21 and 146a. Treatment with this new nutraceutical also prevented age-induced insulin resistance in the liver, gastrocnemius and visceral adipose tissue by decreasing the mRNA levels of inflammatory and oxidative stress markers. Oil mixture + OLE also attenuated the age-induced alterations in vascular function and prevented muscle loss by decreasing the expression of sarcopenia-related markers. In conclusion, treatment with a new nutraceutical based on a mixture of EVOO, AO and OLE is a useful strategy for improving the stability of n-3 PUFA in the final product and to attenuate the cardiometabolic and muscular disorders associated with aging.


2021 ◽  
pp. 1-3
Author(s):  
John F Burd

Obesity and type 2 diabetes are related worldwide epidemics which could be erased with the help of governments and medical communities using tools that are readily available today. Prevailing diet recommendations, which are clearly wrong, are a significant cause of both obesity and type 2 diabetes and have led to the current dire situation. According to the CDC, in the United States alone there are currently 34.2 million people with diabetes of which 30 million have type 2 diabetes. In addition, 88 million Americans have prediabetes (defined as an A1c above 5.7%) which will almost certainly progress to type 2 diabetes if not treated and reversed. The cause of insulin resistance, prediabetes and type 2 diabetes is “glucose toxicity” as explained below, and understanding this medical term is paramount to the case against using insulin for type 2 diabetes. Glucose reacts with all the proteins in the body leading to insulin resistance and type 2 diabetes. Unfortunately, nearly 20% of adults with type 2 diabetes are prescribed insulin injections often in conjunction with oral pharmaceutical medications. Because people with with type 2 diabetes have insulin resistance, prescribing insulin is a very bad idea, since they will need an ever-increasing dosage of insulin as time passes, leading to a lifetime of insulin injections. There is only one product, Lysulin (www.lysulin.com), that targets the cause of insulin resistance and has been proven in double blind, placebo controlled clinical studies to improve insulin resistance and better cell function. The recommend initial treatment for type 2 diabetes should be moderate exercise, intermittent fasting, a low calorie, low carbohydrate ketrogenic diet combined with Lysulin before instituting insulin therapy for type 2 diabetes. By adhering to a ketogenic diet that includes moderate exercise, intermittent fasting and nutritional supplementation with Lysulin, diabetes can be halted and quite possibly reversed. Lysulin is a patented nutritional supplement that contains lysine, zinc, and vitamin C [1]. Double-blind placebo-controlled clinical studies have shown the effectiveness of this nutritional supplement [2, 3].


2019 ◽  
Vol 38 (5) ◽  
pp. 2087-2097 ◽  
Author(s):  
Maricela Rodríguez-Cruz ◽  
Salvador Atilano-Miguel ◽  
Lourdes Barbosa-Cortés ◽  
Mariela Bernabé-García ◽  
Tomas Almeida-Becerril ◽  
...  

2019 ◽  
Vol 6 (1) ◽  
pp. 1796-1803
Author(s):  
Rashmi S. Chouthe ◽  
◽  
Santosh D Shelke ◽  
Rahul P. Kshirsagar ◽  
◽  
...  

2002 ◽  
Vol 3 (3) ◽  
pp. 153-158 ◽  
Author(s):  
Valdemar Grill ◽  
Anneli Björklund

Insulin secretion declines progressively before and during the course of type 2 diabetes. Evidence indicates that this process is, in part, secondary to increased requirement for insulin secretion that is brought about by insulin resistance and by hyperglycemia. The effects of over-secretion extend far beyond a mere reduction of available insulin stores and may cause not only functional but also structural damage. The time is ripe for clinical studies, which explore the therapeutic potential of reducing over-secretion.


2019 ◽  
Vol 39 (02) ◽  
pp. 164-172 ◽  
Author(s):  
Thati Madhusudhan ◽  
Wolfram Ruf

AbstractNutrient excess in obesity drives metabolic reprogramming in multiple tissues involving extensive interorgan and intercellular crosstalk. Experimental and clinical studies show that prolonged nutrient excess often compromises metabolic adaptation propagating proobesogenic and proinflammatory responses. Chronic inflammation further promotes insulin resistance and associated comorbidities. Obesity and type 2 diabetes are characterized by a hypercoagulable state and clinical studies show a strong correlation of markers of coagulation activation in metabolic disorders. Coagulation protease-dependent signalling via protease-activated receptors is intimately associated with inflammation. The experimental evidence supports roles of tissue factor and G protein coupled protease-activated receptor-2 signalling in the regulation of insulin resistance and metabolic inflammation in diet-induced obesity. Likewise, increases in plasminogen activator inhibitor-1 levels and fibrin-driven inflammation promote insulin resistance in obesity. Additionally, impaired thrombomodulin-dependent protein C activation is mechanistically linked to diabetic kidney disease. Given the increased usage of direct oral anticoagulants, understanding the role of specific coagulation proteases in regulation of metabolic inflammation is highly relevant and might provide insights into the design of novel treatment regimens for patients suffering from thromboinflammatory and cardiometabolic disorders.


Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 223
Author(s):  
Kassandra Lanchais ◽  
Frederic Capel ◽  
Anne Tournadre

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by a high prevalence of death due to cardiometabolic diseases. As observed during the aging process, several comorbidities, such as cardiovascular disorders (CVD), insulin resistance, metabolic syndrome and sarcopenia, are frequently associated to RA. These abnormalities could be closely linked to alterations in lipid metabolism. Indeed, RA patients exhibit a lipid paradox, defined by reduced levels of total, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol whereas the CVD risk is increased. Moreover, the accumulation of toxic lipid mediators (i.e., lipotoxicity) in skeletal muscles can induce mitochondrial dysfunctions and insulin resistance, which are both crucial determinants of CVD and sarcopenia. The prevention or reversion of these biological perturbations in RA patients could contribute to the maintenance of muscle health and thus be protective against the increased risk for cardiometabolic diseases, dysmobility and mortality. Yet, several studies have shown that omega 3 fatty acids (FA) could prevent the development of RA, improve muscle metabolism and limit muscle atrophy in obese and insulin-resistant subjects. Thereby, dietary supplementation with omega 3 FA should be a promising strategy to counteract muscle lipotoxicity and for the prevention of comorbidities in RA patients.


Sign in / Sign up

Export Citation Format

Share Document