Organophosphorus Insecticides and Glucose Homeostasis

Joshi, Apurva Kumar Ramesh; Rajini, P.S.

doi:10.5772/28721

Cited by 9 publications

(13 citation statements)

References 61 publications

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“…The mechanisms mediating their propensity to alter glucose homeostasis is attributable to their class (organophosphate compounds) regardless for their chemical structure, toxic potential or whether they are direct or indirect acting OPI. This is clearly evident from a large number of experimental studies that demonstrate hyperglycemic potential of many OPI in various mammalian and non‐mammalian organisms . A hallmark of OPI‐induced hyperglycemia is rapidity of onset and its transient nature.…”

Section: Discussionmentioning

confidence: 97%

Organophosphorus insecticide, monocrotophos, possesses the propensity to induce insulin resistance in rats on chronic exposure 大鼠长期暴露于有机磷杀虫剂—久效磷后可能诱发胰岛素抵抗

Nagaraju

Joshi

Rajini

2014

Journal of Diabetes

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Section: Discussionmentioning

confidence: 97%

Organophosphorus insecticide, monocrotophos, possesses the propensity to induce insulin resistance in rats on chronic exposure 大鼠长期暴露于有机磷杀虫剂—久效磷后可能诱发胰岛素抵抗

Nagaraju

Joshi

Rajini

2014

Journal of Diabetes

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“…Hence, we provided the animals with 10× TMDI dose, which is 47.2 times (Additional file 1: Figure S7A) higher than the acceptable daily intake (FAO/WHO, 1996). In the absence of AChE inhibition during chronic exposure, the mechanism of OP-induced glucose dyshomeostasis is not clearly defined [8, 9]. …”

Section: Discussionmentioning

confidence: 99%

Gut microbial degradation of organophosphate insecticides-induces glucose intolerance via gluconeogenesis

et al. 2017

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BackgroundOrganophosphates are the most frequently and largely applied insecticide in the world due to their biodegradable nature. Gut microbes were shown to degrade organophosphates and cause intestinal dysfunction. The diabetogenic nature of organophosphates was recently reported but the underlying molecular mechanism is unclear. We aimed to understand the role of gut microbiota in organophosphate-induced hyperglycemia and to unravel the molecular mechanism behind this process.ResultsHere we demonstrate a high prevalence of diabetes among people directly exposed to organophosphates in rural India (n = 3080). Correlation and linear regression analysis reveal a strong association between plasma organophosphate residues and HbA1c but no association with acetylcholine esterase was noticed. Chronic treatment of mice with organophosphate for 180 days confirms the induction of glucose intolerance with no significant change in acetylcholine esterase. Further fecal transplantation and culture transplantation experiments confirm the involvement of gut microbiota in organophosphate-induced glucose intolerance. Intestinal metatranscriptomic and host metabolomic analyses reveal that gut microbial organophosphate degradation produces short chain fatty acids like acetic acid, which induces gluconeogenesis and thereby accounts for glucose intolerance. Plasma organophosphate residues are positively correlated with fecal esterase activity and acetate level of human diabetes.ConclusionCollectively, our results implicate gluconeogenesis as the key mechanism behind organophosphate-induced hyperglycemia, mediated by the organophosphate-degrading potential of gut microbiota. This study reveals the gut microbiome-mediated diabetogenic nature of organophosphates and hence that the usage of these insecticides should be reconsidered.Electronic supplementary materialThe online version of this article (doi:10.1186/s13059-016-1134-6) contains supplementary material, which is available to authorized users.

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“…A brief case report article in 1981 detailed two cases admitted after OP exposure and who exhibited hyperglycemia [16]. Glucose serum levels were rapidly lowered after pralidoxime administration, proving the link between poisoning and hyperglycemia [16].…”

Section: Resultsmentioning

confidence: 99%

“…IGF-1 is involved in anabolic and mitogenic processes mediated by GH [25]. Furthermore, IGF-1 is acts as an acute phase response to stress, thus explaining increased values post OP exposure [16,26].…”

Section: Resultsmentioning

confidence: 99%

Effects of Acute Organophosphate Poisoning on Glycemic Profile in Weanling Rats An experimental study

Tomescu¹,

Cobilinschi²,

Băetu³

et al. 2019

Rev. Chim.

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Organophosphates (OP) are frequently used worldwide as pesticides in both agriculture and human households leaving toxic residues in food or living environment. OP act through acetylcholinesterase (AChE) inhibition and acute poisoning carries a higher risk of mortality due to parasympathetic overstimulation. Long-term exposure leads to nervous, hepatic or renal dysfunction. Chlorpyrifos, one of the most commonly used compound appears to cause hyperglycemia, insulin resistance and the risk of developing diabetes after prolonged exposure. The aim of this article was to assess the impact of acute OP poisoning on glycemic status in weanling mice.

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Organophosphorus Insecticides and Glucose Homeostasis

Cited by 9 publications

References 61 publications

Organophosphorus insecticide, monocrotophos, possesses the propensity to induce insulin resistance in rats on chronic exposure 大鼠长期暴露于有机磷杀虫剂—久效磷后可能诱发胰岛素抵抗

Organophosphorus insecticide, monocrotophos, possesses the propensity to induce insulin resistance in rats on chronic exposure 大鼠长期暴露于有机磷杀虫剂—久效磷后可能诱发胰岛素抵抗

Gut microbial degradation of organophosphate insecticides-induces glucose intolerance via gluconeogenesis

Effects of Acute Organophosphate Poisoning on Glycemic Profile in Weanling Rats An experimental study

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