Maternal micronutrient deficiency leads to alteration in the kidney proteome in rat pups

Ahmad, Shadab; Kumar, Kalle Anand; Bhardwaj, Gourav; Lalitha, Anumula; Yadav, Dilip Kumar; Chandak, Giriraj Ratan; Raghunath, Manchala; Sengupta, Shantanu

doi:10.1016/j.jprot.2015.04.035

Cited by 3 publications

(7 citation statements)

References 41 publications

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“…65 Indeed, enriched/differential expression of 27 proteins involved in pathways that regulate amino acid, lipid, and carbohydrate metabolism was observed, and this was restored to control levels after B12 rehabilitation of restricted mothers from parturition. 65,66 In conclusion, maternal and peri-or postnatal folate and/ or vitamin B12 restriction increased visceral adiposity (perhaps due to increased corticosteroid stress), altered lipid metabolism in rat offspring probably by modulating adipocyte function resulting in inflammatory status.…”

Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 94%

“…We also determined the modulation if any, of the 1-carbon pathway/production of SAM in mother/offspring, which is essential for epigenetic regulation of gene expression changes associated with offspring's body composition. [62][63][64][65][66] Unlike the other MN deficiencies studied earlier, it was interesting that dietary folate and/or B12 restriction per se increased body weight, body fat (visceral adiposity), and altered lipid profile in female Wistar rats (mothers) before mating, albeit the differences were significant with only B12 restriction. 62 Also, only the offspring born to vitamin B12-restricted dams had LBW, while those of folate and/ or vitamin B12 restricted dams weighed higher at/from weaning.…”

Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 99%

“…65 Therefore, it appears that modulation of epigenetics and other common mechanisms could underlie/be associated with the maternal MN (folate and/or vitamin B12) restriction-induced phenotypic changes in the offspring. 65,66 Mouse genome is closer to human genome and is rich in CpG islands 67 that undergo methylation/demethylation affecting gene expression and hence mouse is considered a model better suited to assess epigenetic changes. Therefore, studies were conducted in C57BL/6 mice to decipher the underlying/associated epigenetic changes if any.…”

Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 99%

“…70 Thus vitamin B12 restriction appears to alter promoter DNA methylation and/or modulate histone modifying enzyme expression, which in turn regulate the expression of genes involved in important metabolic processes influencing the offspring's phenotype. 66,69,70 That B12 rehabilitation from conception reversed methylation of many of these regions to control levels probably suggests their causal relationship with the metabolic phenotypes. 65,66 Whether or not similar epigenetic alterations underlie the behavioral changes seen in the offspring, remain to be deciphered.…”

Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 99%

“…66,69,70 That B12 rehabilitation from conception reversed methylation of many of these regions to control levels probably suggests their causal relationship with the metabolic phenotypes. 65,66 Whether or not similar epigenetic alterations underlie the behavioral changes seen in the offspring, remain to be deciphered.…”

Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 99%

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Do Maternal Micronutrient Deficiencies Program the Body Composition and Behavior of the Offspring? Probable Underlying Mechanisms

Kalle

Ghosh

Thomas

et al. 2019

Annals of the National Academy of Medical Sciences (India)

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Obesity and noncommunicable diseases (NCDs) like diabetes are epidemic in India. Developmental origins of health and disease hypothesis, based on epidemiological evidence, associates maternal undernutrition and low birth weight (LBW) of the offspring with increased obesity and diabetes in their later life. Considering widespread maternal micronutrient (MN) deficiencies, LBW, and NCDs in India, we tested the hypothesis, “maternal MN deficiency per se programs the offspring for obesity and increases risk for NCDs in their later life” in rodent models. We showed in Wistar rat offspring that maternal MN (single or combined) deficiency per se: (1) increased body fat (visceral fat) and altered lipid metabolism, (2) decreased lean body and fat free mass, and (3) altered muscle function and altered glucose tolerance/metabolism and insulin sensitivity. Rehabilitation prevented vitamin but not mineral restriction-induced changes in offspring, which showed partial mitigation. Increased oxidative/steroid stress, decreased antioxidant status, and inflammatory state were the associated common mechanisms in the offspring. Our attempts to assess the role of epigenetics showed that folate and/or vitamin B12 deficiencies altered mother’s body composition besides that of the offspring. Additionally, in C57BL/6 mice, B12 deficiency-induced anxiety was observed in mothers and offspring. That expressions of histone modifying enzymes in mice brain and promoter methylation of adiponectin, leptin, and 11βHSD1 genes in rat offspring were altered in MN (B12 and Mg) deficiency suggested that altered epigenetics most likely plays a role in maternal MN deficiency-induced changes in body fat/lipid metabolism and anxiety-like behavior in mothers and offspring.

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Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 94%

Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 99%

Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 99%

Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 99%

Section: Deducing the Role Of Stress Epigenetics And 1-carbon Metabmentioning

confidence: 99%

See 3 more Smart Citations

Do Maternal Micronutrient Deficiencies Program the Body Composition and Behavior of the Offspring? Probable Underlying Mechanisms

Kalle

Ghosh

Thomas

et al. 2019

Annals of the National Academy of Medical Sciences (India)

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The metabolic adaptation of the adult offspring after maternal high‐dosed folic acid supplementation based on the proteomics and metabolomics in rats

Kong

Yan

Niu

et al. 2022

Biomedical Chromatography

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The onset of complex diseases at a later stage of life has been linked with maternal folic acid (FA) ingestion. However, little is known regarding the underlying molecular fingerprints of the offspring. We integrated proteomics-metabolomics profiles and analyzed the influence of maternal FA supplementation on the metabolism of adult offspring rats. Twenty pregnant female rats were randomly assigned to a FA supplementation (FolS group, 10 mg/kg FA) or control group (2 mg/kg FA respectively).Such an omics approach revealed that the dopaminergic synapse pathway, tricarboxylic acid cycle and neural development-related metabolites such as glutamic acid and γ-aminobutyric acid were significantly up-regulated in the FolS group, whereas pyruvic acid, oxalic acid and adipic acid were reduced. Maternal FA supplementation can cause alterations of metabolites and protein in the offspring rats.

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Systemic vitamin intake impacting tissue proteomes

Jeong

Vacanti

2020

Nutr Metab (Lond)

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The kinetics and localization of the reactions of metabolism are coordinated by the enzymes that catalyze them. These enzymes are controlled via a myriad of mechanisms including inhibition/activation by metabolites, compartmentalization, thermodynamics, and nutrient sensing-based transcriptional or post-translational regulation; all of which are influenced as a network by the activities of metabolic enzymes and have downstream potential to exert direct or indirect control over protein abundances. Considering many of these enzymes are active only when one or more vitamin cofactors are present; the availability of vitamin cofactors likely yields a systems-influence over tissue proteomes. Furthermore, vitamins may influence protein abundances as nuclear receptor agonists, antioxidants, substrates for post-translational modifications, molecular signal transducers, and regulators of electrolyte homeostasis. Herein, studies of vitamin intake are explored for their contribution to unraveling vitamin influence over protein expression. As a body of work, these studies establish vitamin intake as a regulator of protein abundance; with the most powerful demonstrations reporting regulation of proteins directly related to the vitamin of interest. However, as a whole, the field has not kept pace with advances in proteomic platforms and analytical methodologies, and has not moved to validate mechanisms of regulation or potential for clinical application.

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Maternal micronutrient deficiency leads to alteration in the kidney proteome in rat pups

Cited by 3 publications

References 41 publications

Do Maternal Micronutrient Deficiencies Program the Body Composition and Behavior of the Offspring? Probable Underlying Mechanisms

Do Maternal Micronutrient Deficiencies Program the Body Composition and Behavior of the Offspring? Probable Underlying Mechanisms

The metabolic adaptation of the adult offspring after maternal high‐dosed folic acid supplementation based on the proteomics and metabolomics in rats

Systemic vitamin intake impacting tissue proteomes

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