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Exploring Fluoride’s Role in Diabetes Development: A review.
| Journal of Trace Elements in Medicine and Biology | Thakur R, Rana S, Baltoo R. | 127635.
Diabetes Pancreas Review

Abstract

Purpose:

The element fluorine, which is never found in nature in a free state, is the source of the fluoride ion. When fluoride intake is excessive, it can cause various impairments in living organism. This review aims to assess the relationship between fluoride exposure and glucose metabolism, considering positive, negative, and null findings, with a focus on its potential role in insulin resistance and diabetes-related complications.

Methods:

Numerous studies that have demonstrated changes in blood glucose and insulin variations due to fluoride are included in our analysis on the bases of their relevance. Twenty significant research papers from Pubmed, Google Scholar, and Research Gate are included up to January 2025 using search terms such as “Fluoride,” “Toxicity,” “Diabetes,” “Insulin resistance,” “fluoride and diabetes,” “fluoride and insulin,” “fluoride and blood glucose” in this review. Of the 20 research papers, 14 involve normal organisms unaffected by diabetes or complications connected to the disease, serving as standard animal models, while 5 involve animals exposed to diabetes and 1 is a human population study.

Results:

The findings suggest a negative association between fluoride exposure and diabetes, as studies indicate fluoride’s potential role in impairing glucose homeostasis and increasing insulin resistance. These research studies showed how fluoride affected the participants’ blood sugar and diabetes-related complications.

Conclusion:

This study highlights how important it is to comprehend how fluoride may contribute to diabetes or diabetes-related complications, and it makes recommendations for future research directions that might lead to the discovery of efficient treatment measures to avoid them.

Introduction

The element fluorine is widely distributed in the earth’s crust and interacts easily with other elements to form fluoride salts [1]. In food, water, soil, rocks, and other materials, fluoride is a prevalent environmental contaminant [2]. While fluoride can promote osteoblastic activity and proliferation, which can result in enhanced bone production, it is a necessary trace element for maintaining bone health. On the other hand, consuming too much NaF might hinder the digestion of carbohydrates, which can increase the risk of hyperglycaemia, insulin resistance, and modifications to insulin signalling [3]. In an effort to reduce the amount of F– that people are exposed to through drinking water, the WHO and a few other nations have set F– limits falling between 1 and 1.5 mg/L [4].

Section snippets

Sources of fluoride exposure

Aerosols, food, and cosmetics are some of the ways that fluoride can enter the body. Water consumption is the most common way that humans are overexposed to fluoride (F–) [5], while dietary consumption, including vegetables, cereals, and drinks produced on agricultural land, represents the second potential exposure pathway due to trace levels of F– present in these foods [6]. Since they are raised on soil, these foods easily absorb fluoride. It also relies on the F– content of the water, …

Effect of fluoride on pancreatic islet

The pancreas is a complex organ consists of exocrine and endocrine glands, The endocrine part of the pancreas is formed of the islet Langerhans, which include four types of cells: alpha, beta, delta, and gamma-cells. Beta cells are responsible for the secretion of insulin, a hormone which helps in maintaining blood sugar homeostasis and preventing hyperglycemia [35], [36]. Insulin facilitates glucose uptake by cells, allowing it to be used for energy production or stored for later use. Insulin…

Material and Methods

A thorough search was carried out employing terms like “fluoride,” “toxicity,” “diabetes,” “blood glucose,” and “insulin resistance” “fluoride and diabetes,” “fluoride and insulin,” “fluoride and blood glucose” on PubMed, Google Scholar, and Research Gate as shown in Fig. 2. Studies were selected based on their relevance on the effect of fluoride on blood glucose, insulin resistance, and related metabolic parameters in humans or animal models were considered. Key findings, research design,…

Findings from animal studies (Table- 1, 2)

For example, McGown and Suttie [48] found increased blood glucose levels in NaF treated Sprague-Dawley rats and the effects worsened by epinephrine sensitivity. Similarly, Wistar rats, which had been treated with fluoride and diabetic agents –STZ or alloxan – displayed high glycemia, nephrotoxicity, and decreased glucose uptake [52], [53], [54]. Other research also showed a reduction in the insulin release, uptake and phosphorylation of insulin receptors in rats treated with fluoride [46], [50] …

Findings from Human study (Table- 3)

In humans, Trivedi et al. [43] identified that the endemic fluorosis affected people exhibit reduced glucose tolerance, higher fasting insulin level, and a lower GI ratio, which returned to normal after the removal of fluoride intake. Altogether, these studies highlight fluoride’s significant role in promoting hyperglycemia, insulin resistance, and disruptions in glucose homeostasis….

Findings from animal studies (Tables 1–2)

Summary

Fluoride exposure has been shown to disrupt pancreatic function and glucose metabolism, potentially increasing the risk of diabetes. Animal studies indicate that fluoride alters hormonal secretion from the islets of Langerhans, reducing insulin and glucagon levels, thereby disturbing glucose homeostasis [46], [64], [65]. The severity of hyperglycemia correlates with fluoride dosage, with significant increases noted at doses nearing LD50 levels [48]. Impaired glucose tolerance is prevalent in…

Conclusion

Fluoride exposure leads to pancreatic damage causes oxidative stress, increases inflammatory genes (TNF-a and IL-6), decreases anti-inflammatory genes (IL-10), and alters the architecture of the islets of Langerhans. It also affects the glucose regulation in the body. Similar to the process seen in diabetes, it also suppresses the production of insulin and glucagon, causes insulin resistance, raises blood glucose levels, and reduces glucose tolerance in a dose-dependent way. These results …

Funding sources

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

References (85)