Early-Life Arsenic Exposure, Nutritional Status, and Adult Diabetes Risk

Navas‐Acien, Ana; Spratlen, Miranda J.; Abuawad, Ahlam; LoIacono, Nancy J.; Bozack, Anne K.; Gamble, Mary V.

doi:10.1007/s11892-019-1272-9

Cited by 38 publications

(22 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The transgenerational effects of iAs have not been studied in mammals, although the effect of early‐life iAs exposure on later‐life health has been characterized under the DOHaD paradigm. [ 18–30 ] We focused on an exclusive male‐lineage exposure paradigm. This paradigm excludes most early‐life developmental processes from prenatal or in utero exposures, [ 8 ] which allow us to study transgenerational effects within two generations.…”

Section: Introductionmentioning

confidence: 99%

Inter‐ and Transgenerational Effects of Paternal Exposure to Inorganic Arsenic

Gong

Xue

et al. 2021

Advanced Science

View full text Add to dashboard Cite

The rise of metabolic disorders in modern times is mainly attributed to the environment. However, heritable effects of environmental chemicals on mammalian offsprings' metabolic health are unclear. Inorganic arsenic (iAs) is the top chemical on the Agency for Toxic Substances and Disease Registry priority list of hazardous substances. Here, we assess cross‐generational effects of iAs in an exclusive male‐lineage transmission paradigm. The exposure of male mice to 250 ppb iAs causes glucose intolerance and hepatic insulin resistance in F1 females, but not males, without affecting body weight. Hepatic expression of glucose metabolic genes, glucose output, and insulin signaling are disrupted in F1 females. Inhibition of the glucose 6‐phosphatase complex masks the intergenerational effect of iAs, demonstrating a causative role of hepatic glucose production. F2 offspring from grandpaternal iAs exposure show temporary growth retardation at an early age, which diminishes in adults. However, reduced adiposity persists into middle age and is associated with altered gut microbiome and increased brown adipose thermogenesis. In contrast, F3 offspring of the male‐lineage iAs exposure show increased adiposity, especially on a high‐calorie diet. These findings have unveiled sex‐ and generation‐specific heritable effects of iAs on metabolic physiology, which has broad implications in understanding gene‐environment interactions.

show abstract

Section: Introductionmentioning

confidence: 99%

Inter‐ and Transgenerational Effects of Paternal Exposure to Inorganic Arsenic

Gong

Xue

et al. 2021

Advanced Science

View full text Add to dashboard Cite

show abstract

“…Notably, many animal studies have shown that exposure to arsenic in utero and in the postpartum period increased HOMA-IR in the offspring [ 74 , 75 , 76 , 77 , 78 ]. Considering the subjects in this study were relatively young (average age was approximately 37 years) and the arsenic contamination of tube-well water was first reported in Bangladesh about 30 years ago, a part of our study participants may have undergone prenatal and early-life exposure to arsenic.…”

Section: Discussionmentioning

confidence: 99%

Arsenic Secondary Methylation Capacity Is Inversely Associated with Arsenic Exposure-Related Muscle Mass Reduction

Sarker

Tony

Siddique

et al. 2021

IJERPH

View full text Add to dashboard Cite

Skeletal muscle mass reduction has been implicated in insulin resistance (IR) that promotes cardiometabolic diseases. We have previously reported that arsenic exposure increases IR concomitantly with the reduction of skeletal muscle mass among individuals exposed to arsenic. The arsenic methylation capacity is linked to the susceptibility to some arsenic exposure-related diseases. However, it remains unknown whether the arsenic methylation capacity affects the arsenic-induced reduction of muscle mass and elevation of IR. Therefore, this study examined the associations between the arsenic methylation status and skeletal muscle mass measures with regard to IR by recruiting 437 participants from low- and high-arsenic exposure areas in Bangladesh. The subjects’ skeletal muscle mass was estimated by their lean body mass (LBM) and serum creatinine levels. Subjects’ drinking water arsenic concentrations were positively associated with total urinary arsenic concentrations and the percentages of MMA, as well as inversely associated with the percentages of DMA and the secondary methylation index (SMI). Subjects’ LBM and serum creatinine levels were positively associated with the percentage of DMA and SMI, as well as inversely associated with the percentage of MMA. HOMA-IR showed an inverse association with SMI, with a confounding effect of sex. Our results suggest that reduced secondary methylation capacity is involved in the arsenic-induced skeletal muscle loss that may be implicated in arsenic-induced IR and cardiometabolic diseases.

show abstract

“…Maternal disorders during pregnancy might induce epigenetic modifications in the infant, resulting in dysregulation of β-cell development 28 . Nutrition factors, both pre-and postnatal nutrition, have essential roles in the development of diabetes, as well as the reduced β-cell mass 29,30 . For prenatal nutrition factors, maternal nutrition during pregnancy and intrauterine nutrition is well known to be predominant in health outcomes of offspring.…”

Section: Discussionmentioning

confidence: 99%

Maternal and paternal histories differentially influence risks for diabetes, insulin secretion and insulin resistance in a Chinese population

Kong

Yang

Zhang

et al. 2020

J of Diabetes Invest

View full text Add to dashboard Cite

Aims/Introduction To investigate the differential effects of maternal versus paternal history of diabetes on the risks for diabetes and prediabetes, as well as on insulin secretion and resistance in Chinese individuals. Materials and Methods From the 2007 to 2008 China National Diabetes and Metabolism Disorders Study, 39,244 participants were included and divided into four categories: negative parental history, paternal history only (PH), maternal history only (MH), and both paternal and maternal history. Results The age‐ and sex‐standardized prevalence rates of diabetes in the negative parental history, PH, MH, and both paternal and maternal history groups were 8.59, 12.56, 15.86 and 29.81%, respectively. The prevalence rates of impaired glucose metabolism were 24.13, 25.41, 31.13 and 50.80%, with the prevalence in the MH group being significantly higher than that in the PH group. Compared with that in the FH0 group, the risks of diabetes in the PH, MH, and both paternal and maternal history groups were 2.01‐, 2.67‐ and 6.37‐fold greater, and the risks of impaired glucose metabolism were 1.28‐, 1.65‐ and 3.45‐fold greater. In addition, MH had a significantly greater impact on impaired glucose metabolism than PH (PMHvsPH = 0.0292). Regression analyses suggested MH was associated with homeostatic model assessment for β‐cell function (β[SE] = −0.0910[0.0334], P = 0.0065), insulinogenic index (−0.1866[0.0550], P = 0.0007), homeostatic model assessment for insulin resistance (0.0662[0.0227], P = 0.0036) and Matsuda Index [−0.0716(0.0203), P = 0.0004]. PH was specifically associated with homeostatic model assessment for insulin resistance (0.1343[0.0267], P < 0.0001) and Matsuda Index (−0.1566[0.0243], P < 0.0001), but the effects were stronger than those of MH (PMHvsPH = 0.0431, 0.0054). Conclusions MH and PH differentially influence the risks for diabetes, insulin secretion, and insulin resistance in the Chinese population, suggesting they participate in the pathogenesis of diabetes through different mechanisms.

show abstract

Early-Life Arsenic Exposure, Nutritional Status, and Adult Diabetes Risk

Cited by 38 publications

References 81 publications

Inter‐ and Transgenerational Effects of Paternal Exposure to Inorganic Arsenic

Inter‐ and Transgenerational Effects of Paternal Exposure to Inorganic Arsenic

Arsenic Secondary Methylation Capacity Is Inversely Associated with Arsenic Exposure-Related Muscle Mass Reduction

Maternal and paternal histories differentially influence risks for diabetes, insulin secretion and insulin resistance in a Chinese population

Contact Info

Product

Resources

About