The role of dietary antioxidants in type 2 diabetes and neurodegenerative disorders: An assessment of the benefit profile

Abstract

Healthy diet is vital to cellular health. The human body succumbs to numerous diseases which afflict severe economic and psychological burdens on the patient and family. Oxidative stress is a possible crucial regulator of various pathologies, including type 2 diabetes and neurodegenerative diseases. It generates reactive oxygen species (ROS) that trigger the dysregulation of essential cellular functions, ultimately affecting cellular health and homeostasis. However, lower levels of ROS can be advantageous and are implicated in a variety of signaling pathways. Due to this dichotomy, the terms oxidative "eustress," which refers to a good oxidative event, and "distress," which can be hazardous, have developed. ROS affects multiple signaling pathways, leading to compromised insulin secretion, insulin resistance, and β-cell dysfunction in diabetes. ROS is also associated with increased mitochondrial dysfunction and neuroinflammation, aggravating neurodegenerative conditions in the body, particularly with age. Treatment includes drugs/therapies often associated with dependence, side effects including non-selectivity, and possible toxicity, particularly in the long run. It is imperative to explore alternative medicines as an adjunct therapy, utilizing natural remedies/resources to avoid all the possible harms. Antioxidants are vital components of our body that fight disease by reducing oxidative stress or nullifying the excess toxic free radicals produced under various pathological conditions. In this review, we focus on the antioxidant effects of components of dietary foods such as tea, coffee, wine, oils, and honey and the role and mechanism of action of these antioxidants in alleviating type 2 diabetes and neurodegenerative disorders. We aim to provide information about possible alternatives to drug treatments used alone or combined to reduce drug intake and encourage the consumption of natural ingredients at doses adequate to promote health and combat pathologies while reducing unwanted risks and side effects.

Keywords: Antioxidants; Diet; Neurodegenerative diseases; Reactive oxygen species; Therapeutics; Type 2 diabetes.

Fig. 1

Classification of antioxidants based on their origin. This includes natural, endogenous, enzymatic, non-enzymatic, exogenous and synthetic antioxidants that help inhibit the activity of toxic oxidative radicals, including various Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS).

Fig. 2

Precise summary of the effect and action of dietary antioxidants in type 2 diabetes. These include the effect of Tea, Coffee, Vitamins, Red wine, Honey and common Herbs and Oils, highlighting the precise effect and the pathways that they might target. Inc (increased), Dec (decreased), Red (reduced), AO (antioxidants), Heme oxygenase (HO-1), Superoxide dismutase (SOD), catalase (CAT), matrix metalloproteinases (MMPs), Hemoglobin A1c (HbA1c), nuclear factor erythroid 2-related factor (NRF2), Nuclear Factor kappa B (NF-κB), peroxisome proliferator-activated receptor gamma (PPAR-γ), Protein Kinase B (Akt), AMP-activataed protein kinase (AMPK), extracellular regulated kinase (ERK), c-Jun N-terminal linase (JNK), phosphatidylinositol 3-kinase (PI3K), glycogen synthase kinase 3 Beta (GSK3B), ROS (Reactive Oxygen Species). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Fig. 3

Overview of the effect of oxidative stress in neurodegenerative diseases and the role of antioxidants. Upward red arrow (increase), Downward green arrow (decrease), and thin blue arrows indicate the passing of various classes of antioxidant molecules, including polyphenols, flavonoids, amino acids, curcumin, and more across the Blood-brain barrier (BBB), reactive oxygen species (ROS), reactive nitrogen species (RNS). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)