Artificial sweeteners (AS) were first introduced as food additives or sugar substitutes more than a century ago with the intention of supplying sweet taste without the high caloric content of sugar. AS are employed in place of sucrose (table sugar) with the view of providing sweetness to foodstuffs and bottled drinks. The end-users, along with producers of canned food and drinks, have long been captivated by the idea of replacing sugar in food items with AS. Foods that use AS in place of sugar have become increasingly common during the past decade. Artificial sugars are normally many folds sweeter than normal sugar possessing low or zero calories, which confers to their public appeal for the management of overweight issues. Due to this, they are, at present, employed by many individuals all over the world, without knowing the potential hazards associated with them. The use of AS in obese, diabetic, and/or heart patients or patients with metabolic syndrome has been approved with caution by The American Heart Association and American Diabetes Association (ADA) as a low-calorie option for normal sugar. Judicious use of sugar substitutes can help in maintaining blood glucose, calories and body weight, thus automatically minimizing the risk factors of diabetes and heart disease. Since the day of their discovery and approval, their safety issue has been quite controversial and debated extensively. The article follows an exhaustive review discussing the history, uses, and chemical features of a wide variety of sweeteners with a focus on their association with diabetes and potential adverse effects on the body.
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http://dx.doi.org/10.2174/1573399818666220429083052 | DOI Listing |
Arch Microbiol
January 2025
Tecnológico Nacional de México, Instituto Tecnológico de Morelia, 58120, Morelia, Mexico.
The metabolites gluconic acid, 5-ketogluconic acid, proline, and glutamic acid, produced by Pseudomonas reptilivora B-6bs, are industrially important, particularly in food and pharmaceutical sectors. However, producing these metabolites involves biotin supplementation to enhance yields, which is an expensive additive, and reducing its use can significantly lower production costs. Thus, This study aimed to enhance the production of gluconic acid, 5-ketogluconic acid, proline, and glutamic acid without biotin supplementation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Indian Institute of Technology, Gandhinagar, India.
Background: Diabetes is a modifiable risk factor for Alzheimer's disease, and GLUT4, an insulin-dependent transporter, plays a crucial role in insulin-resistant conditions and, consequently, in diabetes development. The study aimed to investigate the relationship between tau pathology and insulin resistance by quantifying GLUT4 expression and glucose concentration.
Method: Initially, SH-SY5Y cells underwent transfection with either a wild-type tau plasmid or a mutant tau plasmid.
Alzheimers Dement
December 2024
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Background: While disease-modifying treatments that reduce Aβ have been recently approved by the FDA, the identification of novel therapeutic targets and strategies that target underlying mechanisms to delay the AD development are still needed. Abnormal brain energy homeostasis and mitochondria dysfunction are observed early in AD. Therefore, the development of treatments to restore these defects could be beneficial.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Columbia University, New York, NY, USA.
Background: Genome-wide association studies (GWAS) have identified genetic loci that robustly associate with Alzheimer's Disease (AD), many of which are preferentially or exclusively expressed in innate immune cells. Among the identified AD risk genes is CD33: a transmembrane, sialic acid-binding protein expressed on the surface of myeloid cells including microglia, the innate immune cells of the CNS. The function of microglia is highly responsive to and regulated by metabolic changes, which allows them to rapidly change phenotype and maintain brain health.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kentucky, Lexington, KY, USA.
Background: Alzheimer's disease is defined by the pathological aggregation of amyloid-beta and hyperphosphorylated tau. AD patients often exhibit other symptoms like metabolic and sleep dysfunction. Currently, it is unclear if impairments are a cause or consequence of Aβ or tau aggregation.
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