Synthesis of novel 5-(2,5-bis(2,2,2-trifluoroethoxy)phenyl)-1,3,4-oxadiazole-2-thiol derivatives as potential glucosidase inhibitors.

Significance: Type 2 diabetes, which is related to oxidative stress and mitochondrial dysfunction, is one of the most prevalent diseases in the world. In the last decade, alterations in autophagy have been shown to play a fundamental role in the development and control of type 2 diabetes. Furthermore, mitophagy has been recognised as a key player in eliminating dysfunctional mitochondria in this disease. Recent advances: Recently, much progress has been made in understanding the molecular events associated with oxidative stress, mitochondrial dysfunction, and alterations in autophagy and mitophagy in type 2 diabetes. Critical issue: Despite increasing evidence of a relationship between mitochondrial dysfunction, oxidative stress, and alterations of autophagy and mitophagy and their role in the pathophysiolology of type 2 diabetes, effective therapeutic strategies to combat the disease through targeting mitochondria, autophagy and mitophagy are yet to be implemented. Future directions: This review provides a wide perspective of the existing literature concerning the complicated interplay between autophagy, mitophagy and mitochondrial dysfunction in type 2 diabetes. Furthermore, potential therapeutic targets based on these molecular mechanisms are explored.

Mitochondrial dysfunction and mitophagy in type 2 diabetes: pathophysiology and therapeutic targets.

Excessive sugar consumption is a risk factor for the development of several disorders, including metabolic, cardiovascular, neurological conditions and even some cancers, and has been linked to increased morbidity and mortality. The popularization of the typical Western diet, featured by an excessive intake of saturated fats and added sugars and a low consumption of unprocessed fruits, vegetables and fiber, may directly affect the composition and functionality of the gut microbiota, staggering the balance of the intestinal microbiome that ultimately culminates into gut dysbiosis. Although added sugars in the form of nutritive and non-nutritive sweeteners are generally considered as safe, a growing body of evidence correlate their consumption with adverse effects on gut microbial ecosystem; namely an abnormal synthesis of short-chain fatty acids, altered intestinal barrier integrity and chronic inflammation that often fuel a panoply of metabolic conditions. Accordingly, this work revisited the available preclinical evidence concerning the impact of different types of dietary sugars—nutritive and non-nutritive sweeteners—on gut microbiota and metabolic health. Future research should consider gender and species vulnerability when the impact of such substances on GM community and metabolic health is scrutinized in order to guide their adequate use at doses relevant to human use. 

/pdf/impact-of-dietary-sugars-on-gut-microbiota-and-metabolic-k32po589.pdf

Impact of Dietary Sugars on Gut Microbiota and Metabolic Health

With the rapid rise in prevalence, diabetes mellitus is one of the leading causes of mortality worldwide. Impaired cellular glucose transport is a major contributor to diabetes progression and, thus, an important target for treatment. Functional foods are a rich source of antidiabetic agents. These compounds target multiple physiological contributors to diabetes with lower risk for side effects. This perspective highlights recent advances in food-derived compounds that regulate the gene expression or activity of glucose transport proteins (SGLT1, SGLT2, GLUT1, GLUT2, and GLUT4) and provides insights for future research on targeting the transporters as a promising antidiabetic mechanism of nutraceutical compounds. 

Targeting Glucose Transport Proteins for Diabetes Management: Regulatory Roles of Food-Derived Compounds

18:0 Lyso PC, a natural product with potential PPAR-γ agonistic activity, plays hypoglycemic effect with lower liver toxicity and cardiotoxicity in db/db mice.

Type 2 diabetes mellitus (T2DM) accounts for >90% of the cases of diabetes in adults. Resistance to insulin action is the major cause that leads to chronic hyperglycemia in diabetic patients. T2DM is the consequence of activation of multiple pathways and factors involved in insulin resistance and β-cell dysfunction. Also, the etiology of T2DM involves the complex interplay between genetics and environmental factors. This interplay can be governed efficiently by lifestyle modifications to achieve better management of diabetes. The present review aims at discussing the major factors involved in the development of T2DM that remain unfocussed during the anti-diabetic therapy. The review also focuses on lifestyle modifications that are warranted for the successful management of T2DM. In addition, it attempts to explain flaws in current strategies to combat diabetes. The employability of phytoconstituents as multitargeting molecules and their potential use as effective therapeutic adjuvants to first line hypoglycemic agents to prevent side effects caused by the synthetic drugs are also discussed.

/pdf/management-of-type-2-diabetes-current-strategies-unfocussed-2jdbs6vdlq.pdf

Management of Type 2 Diabetes: Current Strategies, Unfocussed Aspects, Challenges, and Alternatives

Saroglitazar and Hepano treatment offers protection against high fat high fructose diet induced obesity, insulin resistance and steatosis by modulating various class of hepatic and circulating lipids.

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Management of Type 2 Diabetes: Current Strategies, Unfocussed Aspects, Challenges, and Alternatives

Saroglitazar and Hepano treatment offers protection against high fat high fructose diet induced obesity, insulin resistance and steatosis by modulating various class of hepatic and circulating lipids.