Possible dietary factors in the induction of diabetes and its inheritance in man, with studies in mice

Stowers, J. M.; Ewen, Stanley B. W.

doi:10.1079/pns19910038

Cited by 6 publications

(5 citation statements)

References 20 publications

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“…The induction of IGT in progeny of nitrosamine-treated animals is unlikely to be due to placental transfer, since clearance of nitrosamines from tissues takes less than 24 h, though it is slower from the testes [9]. In addition mating began 2 weeks after completion of test feeding and second F1 litters contained diabetic offspring from Group 2 betel-fed adults, as reported with other nitrosamine-induced diabetes [19]. The major abnormalities reported in the heads of spermatozoa 30 days after completion of 5 days administration of pan masala (a betel-nut containing snack) to adult mice [20], and the damage to chromosomes in circulating lymphocytes in man and mouse following betel consumption suggests a nuclear mutation should be considered [21], though the more rapid rates of mitochondrial mutation would provide a mechanism for the marked changes in disease incidence between generations [22].…”

Section: Discussionmentioning

confidence: 63%

Betel nut (Areca catechu) consumption and the induction of glucose intolerance in adult CD1 mice and in their F1 and F2 offspring

1994

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SummaryMany mutagenic nitroso compounds are also diabetogenic. Betel-nut (Areca catechu) chewing populations have an increased incidence of foregut cancers related to betel-nut nitrosamines which suggests that betel consumption could be diabetogenic. Young adult CD1 mice with a low spontaneous incidence of diabetes were fed betel nut in standard feed for 2~5 days. Single point (90 min) intra-peritoneal glucose tolerance tests were used to follow glucose tolerance up to 6 months of age. Glucose intolerance was defined as over 3 SD above mean control values. Glucose intolerance was found in 3 of 51 male and 4 of 33 female adult mice which were fed the betel diet (p < 0.01). Studies on the progeny of these mice are presented separately for animals studied in Aberdeen (Group 1) and London (Group2). In matings of Group 1 betel-fed parents glucose intolerance was found in 4 of 25 male and 1 of 22 female F1 offspring, with significant hyperglycaemia in F1 males born to hyperglycaemic but not to normoglycaemic mothers (p < 0.01). In the F2 generation 4 of 23 males and 1 of 16 females and in the F3 generation 1 of 16 males and 0 of 20 females were glucose intolerant. In the Group 2 studies where betel-fed parents were mated to normal controls glucose intolerance was found in 10 of 35 male and 10 of 33 female F1 progeny (p < 0.005), and mean islet areas were increased in offspring of betel-fed parents (p < 0.001). The total incidence of glucose intolerance in F1 progeny from studies in Groups 1 and 2 was 14 of 60 males and 11 of 55 females (p < 0.005). Insulin dependence did not develop in the glucose-intolerant betel-fed animals or their descendants; affected animals appearing well built and active. The development of glucose intolerance in F1 offspring was not dependent on maternal glucose intolerance or on maternal betel-feeding, and 90-min glucose levels of F1 offspring were directly related to paternal but not to maternal glycaemia (p < 0.01). Our findings suggest that betelnut (Areca) consumption may be diabetogenic and induce an inheritable abnormality. The hypothesis is of interest in view of the widespread habit of betel consumption and of the strategies known to inhibit the induction of experimental diabetes by diabetogenic nitroso compounds. [Diabetologia (1994) 37: 49-55]

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Section: Discussionmentioning

confidence: 63%

Betel nut (Areca catechu) consumption and the induction of glucose intolerance in adult CD1 mice and in their F1 and F2 offspring

1994

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“…In 1973-1982 the mean annual incidence per 100,000 for the Norwegian west coast counties was 19.7 [5] compared to 8.0 for 1970-1979 in Iceland. This striking difference may imply a causative role for environmental factors that are not related to latitude or ambient temperature [23][24][25][26].…”

Section: Discussionmentioning

confidence: 99%

Incidence and prevalence of Type 1 (insulin-dependent) diabetes mellitus in Icelandic children 1970?1989

Helgason

Daníelsen

Þórsson³

1992

Diabetologia

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Through use of primary and secondary data sources for registration and validation, the incidence and prevalence of Type 1 (insulin-dependent) diabetes mellitus in children aged 0-14 years in Iceland has been completely ascertained for the years 1970-1989. The age-adjusted mean annual incidence per 100,000 for the 20-year period was 9.4 (95% confidence interval 7.8-11.3); similar for boys (9.9; 7.7-12.7) and girls (8.8; 6.7-11.5). Between 1970-1979 the incidence was 8.0 (6.0-10.6) and between 1980-1989 it was comparable at 10.8 (8.4-13.8) (p greater than 0.10). By Poisson regression analysis the variation in incidence was related to age at diagnosis (p less than 0.001), while a linear trend for calendar year at diagnosis did not reach statistical significance (p = 0.07). A quadratic curve, however, better described the temporal variation in incidence (p less than 0.05). The total prevalence per 1,000 by the end of 1979 and 1989 was similar, 0.45 (0.30-0.65) and 0.57 (0.40-0.79), respectively. In conclusion, this study confirms that both the incidence and prevalence of childhood Type 1 diabetes in Iceland are low compared to the other Nordic countries. The findings may suggest a causative role for environmental factors that are not related to latitude or ambient temperature.

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“…Data are presented as the mean±SD from three independent experiments. a p<0.001, b p<0.01, c p<0.05 (Stowers and Ewen 1991). This report let Boucher et al (1994) consider the betel nut as a diabetogenic substance because the betel nut is also a potent source and precursor of nitrosamines.…”

Section: Discussionmentioning

confidence: 88%

Betel nut extract and arecoline block insulin signaling and lipid storage in 3T3-L1 adipocytes

Hsieh

Hsieh²,

et al. 2011

Cell Biol Toxicol

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According to several population-based studies, betel nut chewing is associated with metabolic syndrome and diabetes in British South Asians and Taiwanese. However, the underlying molecular mechanism is not yet clear. Arecoline is an alkaloid-type natural product found in betel nuts. Our aim was to clarify the influence of betel nut extract and arecoline on lipid accumulation and insulin signaling in adipocytes. We found that betel nut extract and arecoline blocked lipid storage in 3T3-L1 adipocytes. The possible mechanism may function by inhibiting the expression of the insulin receptor, glucose transporter-4, fatty acid synthase, and the lipid droplet proteins perilipin and adipophilin. In addition, betel nut extract and arecoline increased the basal level of IRS-1 serine(307) phosphorylation and decreased insulin-stimulated IRS-1 tyrosine, Akt, and PI3 kinase phosphorylation. In conclusion, betel nut extract and arecoline have diabetogenic potential on adipocytes that may result in insulin resistance and diabetes at least in part via the obstruction of insulin signaling and the blockage of lipid storage.

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Possible dietary factors in the induction of diabetes and its inheritance in man, with studies in mice

Cited by 6 publications

References 20 publications

Betel nut (Areca catechu) consumption and the induction of glucose intolerance in adult CD1 mice and in their F1 and F2 offspring

Betel nut (Areca catechu) consumption and the induction of glucose intolerance in adult CD1 mice and in their F1 and F2 offspring

Incidence and prevalence of Type 1 (insulin-dependent) diabetes mellitus in Icelandic children 1970?1989

Betel nut extract and arecoline block insulin signaling and lipid storage in 3T3-L1 adipocytes

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