The use of combined high-fructose diet and glyphosate to model rats type 2 diabetes symptomatology

Kale, Oluwafemi Ezekiel; Vongdip, Mary; Ogundare, Temitope Funmi; Osilesi, Odutola

doi:10.1080/15376516.2020.1845889

Cited by 10 publications

(2 citation statements)

References 59 publications

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“…T1DM is associated with an increased risk of amyotrophic lateral sclerosis (ALS) in people aged < 50 years of age [ 166 ], with streptozotocin-induced T1DM also leading to neuromuscular junction retraction and muscle atrophy [ 167 ]. There also seems genome-wide genetic overlaps between T1DM and ALS [ 168 ], whilst glyphosate-based herbicides, a proposed risk factor for ALS [ 7 ], induces a T2DM phenotype when combined with a high fructose diet [ 169 ]. Chronic glyphosate causes severe degeneration in pancreatic acinar cells and islets of Langerhans [ 170 ].…”

Section: Future Researchmentioning

confidence: 99%

Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the ‘Bystander’ Activation of Memory CD8+ T Cells

Anderson¹

2023

IJMS

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Type 1 diabetes mellitus (T1DM) arises from the failure of pancreatic β-cells to produce adequate insulin, usually as a consequence of extensive pancreatic β-cell destruction. T1DM is classed as an immune-mediated condition. However, the processes that drive pancreatic β-cell apoptosis remain to be determined, resulting in a failure to prevent ongoing cellular destruction. Alteration in mitochondrial function is clearly the major pathophysiological process underpinning pancreatic β-cell loss in T1DM. As with many medical conditions, there is a growing interest in T1DM as to the role of the gut microbiome, including the interactions of gut bacteria with Candida albicans fungal infection. Gut dysbiosis and gut permeability are intimately associated with raised levels of circulating lipopolysaccharide and suppressed butyrate levels, which can act to dysregulate immune responses and systemic mitochondrial function. This manuscript reviews broad bodies of data on T1DM pathophysiology, highlighting the importance of alterations in the mitochondrial melatonergic pathway of pancreatic β-cells in driving mitochondrial dysfunction. The suppression of mitochondrial melatonin makes pancreatic β-cells susceptible to oxidative stress and dysfunctional mitophagy, partly mediated by the loss of melatonin’s induction of PTEN-induced kinase 1 (PINK1), thereby suppressing mitophagy and increasing autoimmune associated major histocompatibility complex (MHC)-1. The immediate precursor to melatonin, N-acetylserotonin (NAS), is a brain-derived neurotrophic factor (BDNF) mimic, via the activation of the BDNF receptor, TrkB. As both the full-length and truncated TrkB play powerful roles in pancreatic β-cell function and survival, NAS is another important aspect of the melatonergic pathway relevant to pancreatic β-cell destruction in T1DM. The incorporation of the mitochondrial melatonergic pathway in T1DM pathophysiology integrates wide bodies of previously disparate data on pancreatic intercellular processes. The suppression of Akkermansia muciniphila, Lactobacillus johnsonii, butyrate, and the shikimate pathway—including by bacteriophages—contributes to not only pancreatic β-cell apoptosis, but also to the bystander activation of CD8+ T cells, which increases their effector function and prevents their deselection in the thymus. The gut microbiome is therefore a significant determinant of the mitochondrial dysfunction driving pancreatic β-cell loss as well as ‘autoimmune’ effects derived from cytotoxic CD8+ T cells. This has significant future research and treatment implications.

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Section: Future Researchmentioning

confidence: 99%

Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the ‘Bystander’ Activation of Memory CD8+ T Cells

Anderson¹

2023

IJMS

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“…The review identi ed four potential mechanisms leading to IR: glucose metabolism, lipotoxic effect, in ammation, and oxidative stress. For glucose metabolism, a study showed that glyphosate combined with a high-fructose diet (FRC) could increase FBG and induce T2DM in rats (Kale, Vongdip, et al, 2021). Recent research also found that plasma residues of OPs were positively associated with HbA1c in mice and gut microbial degradation of OPs could promote glucose intolerance via gluconeogenesis (Velmurugan, Ramprasath, et al, 2017).…”

mentioning

confidence: 99%

Associations between urine glyphosate and diabetes mellitus in the U.S. general adult: A cross-sectional study from NHANES program

Huang

Chen

et al. 2023

Preprint

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Background Glyphosate-based herbicides (GBHs) are used extensively around the world and have become the leading agrochemicals. However, study about the association between glyphosate exposure and diabetes is scarce. This study used four years of NHANES data (2013–2016) to further investigate the association. Methods A total of 2,806 participants were enrolled in this cross-sectional study. The baseline information and urine glyphosate levels in diabetic and non-diabetic groups were compared. We also divided urine glyphosate levels into tertiles. Three models were developed using weighted logistic regression. Further subgroup analyses based on categorical variables were also conducted. Results Urine glyphosate levels were 0.35ng/ml in people with diabetes and 0.44ng/ml in participants without diabetes (P < 0.05). Regardless of adjustment, the highest glyphosate level in the tertile3 group was significantly linked with an elevated risk of diabetes (OR 1.595, 95% CI 1.016–2.504, P = 0.043) compared to the tertile1 group. Subgroup analyses suggested that the associations were constant in participants who were male, older age (60–100), had a college degree, income ratio = 5, BMI > 30, and smoking. Conclusions This study provides new evidence that glyphosate exposure was associated with a higher risk of diabetes in the American general adult population.

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Associations between urinary glyphosate and diabetes mellitus in the US general adult: a cross-sectional study from NHANES 2013–2016

Qi,

Huang,

Chen

et al. 2023

Environ Sci Pollut Res

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The use of combined high-fructose diet and glyphosate to model rats type 2 diabetes symptomatology

Cited by 10 publications

References 59 publications

Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the ‘Bystander’ Activation of Memory CD8+ T Cells

Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the ‘Bystander’ Activation of Memory CD8+ T Cells

Associations between urine glyphosate and diabetes mellitus in the U.S. general adult: A cross-sectional study from NHANES program

Associations between urinary glyphosate and diabetes mellitus in the US general adult: a cross-sectional study from NHANES 2013–2016

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