The inhibitoty effect of DDT on insulin secretion in mice

Yau, E. T.; Mennear, John H.

doi:10.1016/0041-008x(77)90179-x

Cited by 33 publications

(13 citation statements)

References 9 publications

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“…Similarly, adult rodents exposed to high doses of DDT had impaired insulin secretion, glucose intolerance, and elevated gluconeogenesis [63], [64]. Here we find that female mice perinatally exposed to low doses of DDT and subsequently fed a HFD in adulthood developed impaired glucose tolerance, increased fasting insulin, and HOMA-IR, indicative of insulin resistance and increased risk for T2D.…”

Section: Discussionsupporting

confidence: 50%

Perinatal Exposure of Mice to the Pesticide DDT Impairs Energy Expenditure and Metabolism in Adult Female Offspring

et al. 2014

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Dichlorodiphenyltrichloroethane (DDT) has been used extensively to control malaria, typhus, body lice and bubonic plague worldwide, until countries began restricting its use in the 1970s. Its use in malaria control continues in some countries according to recommendation by the World Health Organization. Individuals exposed to elevated levels of DDT and its metabolite dichlorodiphenyldichloroethylene (DDE) have an increased prevalence of diabetes and insulin resistance. Here we hypothesize that perinatal exposure to DDT disrupts metabolic programming leading to impaired metabolism in adult offspring. To test this, we administered DDT to C57BL/6J mice from gestational day 11.5 to postnatal day 5 and studied their metabolic phenotype at several ages up to nine months. Perinatal DDT exposure reduced core body temperature, impaired cold tolerance, decreased energy expenditure, and produced a transient early-life increase in body fat in female offspring. When challenged with a high fat diet for 12 weeks in adulthood, female offspring perinatally exposed to DDT developed glucose intolerance, hyperinsulinemia, dyslipidemia, and altered bile acid metabolism. Perinatal DDT exposure combined with high fat feeding in adulthood further impaired thermogenesis as evidenced by reductions in core temperature and in the expression of numerous RNA that promote thermogenesis and substrate utilization in the brown adipose tissue of adult female mice. These observations suggest that perinatal DDT exposure impairs thermogenesis and the metabolism of carbohydrates and lipids which may increase susceptibility to the metabolic syndrome in adult female offspring.

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Section: Discussionsupporting

confidence: 50%

Perinatal Exposure of Mice to the Pesticide DDT Impairs Energy Expenditure and Metabolism in Adult Female Offspring

et al. 2014

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“…This may suggest that long-term DDT exposure aected glucose metabolism or insulin production in these monkey species. This ®nding is in keeping with earlier reports on rodents, showing that exposure to DDT lowered blood glucose levels in rats (Berdanier and de Dennis 1977) and inhibited insulin secretion in mice (Yau and Mennear 1977). The question then arises as to whether there is a link between diabetes or hypoglycemia and the development of malignant tumors in the DDT monkeys.…”

Section: Discussionsupporting

confidence: 67%

Effects of long-term oral administration of DDT on nonhuman primates

Takayama¹,

Sieber²,

Dalgard

et al. 1999

Journal of Cancer Research and Clinical Oncology

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Because of reports on tumorigenic activity in different animal species exposed to DDT a decision was made in 1969 to evaluate the long-term effects of DDT on 24 cynomolgus and rhesus monkeys. DDT (20 mg/kg) was given in the diet for 130 months, followed by an observation period that ended in 1994. The two cases of malignant tumor detected in the DDT group included a metastatic hepatocellular carcinoma in a 233-month-old male and a well-differentiated adenocarcinoma of the prostate in a 212-month-old monkey. Benign tumors detected in the DDT group included three cases of leiomyoma, two of which were uterine and one, esophageal. No tumor was detected in the control group of 17 monkeys. Fatty changes in the liver were observed in 52.9% of the DDT group and 29.4% of the control group. More specific signs of hepatotoxicity were documented microscopically in seven DDT monkeys. Severe tremors and histological evidence of CNS and spinal cord abnormalities were observed in six DDT monkeys. The present findings show clear evidence of hepatic and CNS toxicity following long-term DDT administration to cynomolgus and rhesus monkeys. However, the two cases involving malignant tumors of different types are inconclusive with respect to a carcinogenic effect of DDT in nonhuman primates.

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“…2,3,7,8-tetrachlorodibenzodioxin (TCDD) reduces glucose-stimulated insulin secretion (GSIS) in isolated islets [415, 456, 457]. Similarly, DDT impairs both GSIS as well as insulin secretion in response to tolbutamide (a pharmacological insulin secretagogue) [458].…”

Section: Mdcs and Metabolism-relevant Diseasesmentioning

confidence: 99%

“…Adult mice exposed to TCDD exhibited reduced glucose-stimulated insulin release without concomitant hyperglycemia, an effect that was absent in AhR-null mice [456]. Furthermore, TCDD-exposed rats had islets depleted of insulin [415], similar to the depletion of secretory granules observed with chronic exposure to PCBs [475].…”

Section: Mdcs and Metabolism-relevant Diseasesmentioning

confidence: 99%

Metabolism disrupting chemicals and metabolic disorders

Heindel

Blumberg

Cave

et al. 2017

Reproductive Toxicology

848

651

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The recent epidemics of metabolic diseases, obesity, type 2 diabetes(T2D), liver lipid disorders and metabolic syndrome have largely been attributed to genetic background and changes in diet, exercise and aging. However, there is now considerable evidence that other environmental factors may contribute to the rapid increase in the incidence of these metabolic diseases. This review will examine changes to the incidence of obesity, T2D and non-alcoholic fatty liver disease (NAFLD), the contribution of genetics to these disorders and describe the role of the endocrine system in these metabolic disorders. It will then specifically focus on the role of endocrine disrupting chemicals (EDCs) in the etiology of obesity, T2D and NAFLD while finally integrating the information on EDCs on multiple metabolic disorders that could lead to metabolic syndrome. We will specifically examine evidence linking EDC exposures during critical periods of development with metabolic diseases that manifest later in life and across generations.

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The inhibitoty effect of DDT on insulin secretion in mice

Cited by 33 publications

References 9 publications

Perinatal Exposure of Mice to the Pesticide DDT Impairs Energy Expenditure and Metabolism in Adult Female Offspring

Perinatal Exposure of Mice to the Pesticide DDT Impairs Energy Expenditure and Metabolism in Adult Female Offspring

Effects of long-term oral administration of DDT on nonhuman primates

Metabolism disrupting chemicals and metabolic disorders

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