Maternal dietary chromium restriction programs muscle development and function in the rat offspring

Padmavathi, Inagadapa J.N.; Rao, K. R.; Lagishetty, Venu; Ismail, Azman; Raghunath, Manchala

doi:10.1258/ebm.2009.009199

Cited by 14 publications

(13 citation statements)

References 46 publications

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“…Although much work needs to be done to decipher the underlying/associated mechanism(s), they have unequivocally demonstrated the effects of maternal CrR per se in programming the offspring to glucose intolerance and IR and the possible involvement of increased oxidative stress in the process. Taken together with our earlier demonstration of increased body fat%, especially the visceral adiposity (Padmavathi et al 2010a) and decreased myogenesis and altered muscle function in CrR offspring (Padmavathi et al 2010b), the present findings appear to suggest the probable predisposal of the CrR offspring to type 2 diabetes in their later life.…”

Section: Discussionsupporting

confidence: 84%

Impact of maternal chromium restriction on glucose tolerance, plasma insulin and oxidative stress in WNIN rat offspring

Padmavathi¹,

Rao²,

Raghunath³

2011

Journal of Molecular Endocrinology

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Robust evidence suggests that nutritional insult during fetal development could program the offspring to glucose intolerance, impaired insulin response and insulin resistance (IR). Considering the importance of chromium (Cr) in maintaining carbohydrate metabolism, this study determined the effect of maternal Cr restriction (CrR) on glucose metabolism and plasma insulin in Wistar/NIN (WNIN) rat offspring and the associated biochemical and/or molecular mechanisms. Female, weanling WNIN rats received ad libitum for 12 weeks, a control diet or the same with 65% restriction of Cr and mated with control males. Some of the Cr-restricted dams were rehabilitated from conception or parturition and their pups weaned on to control diet. At the time of weaning, half of the Cr restricted offspring were rehabilitated to control diet while others continued on Cr-restricted diet. Maternal CrR increased fasting plasma glucose, fasting insulin, homeostasis model assessment of IR, and area under the curve of glucose and insulin during oral glucose tolerance test in the offspring. Expression and activity of rate-limiting enzymes of glucose metabolism were comparable among different groups and expression of genes involved in insulin secretion was increased albeit in male offspring whereas antioxidant enzyme activities were decreased in offspring of both genders. Rehabilitation, in general, corrected the changes albeit partially. Maternal dietary CrR induced IR, impaired glucose tolerance in WNIN rat offspring and was associated with increased oxidative stress, which may predispose them to type 2 diabetes in their later life.

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Section: Discussionsupporting

confidence: 84%

Impact of maternal chromium restriction on glucose tolerance, plasma insulin and oxidative stress in WNIN rat offspring

Padmavathi¹,

Rao²,

Raghunath³

2011

Journal of Molecular Endocrinology

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“…These data correlate well with human studies showing that iron supplementation during pregnancy leads to a higher mean birth weight and reduced incidence of low birth weight infants [78] . Maternal chromium restriction significantly increased body weight and fat percentage, especially central adiposity, in both male and female rat offspring [79,80] . Restricted vitamin intake during pregnancy has been shown to increase the phenotypic expression of obesity and components of the metabolic syndrome in both female and male rats fed a post-weaning obesogenic diet [81] .…”

Section: Maternal Undernutritionmentioning

confidence: 95%

Developmental programming of the metabolic syndrome - critical windows for intervention

Vickers

2011

WJG

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Metabolic disease results from a complex interaction of many factors, including genetic, physiological, behavioral and environmental influences. The recent rate at which these diseases have increased suggests that environmental and behavioral influences, rather than genetic causes, are fuelling the present epidemic. In this context, the developmental origins of health and disease hypothesis has highlighted the link between the periconceptual, fetal and early infant phases of life and the subsequent development of adult obesity and the metabolic syndrome. Although the mechanisms are yet to be fully elucidated, this programming was generally considered an irreversible change in developmental trajectory. Recent work in animal models suggests that developmental programming of metabolic disorders is potentially reversible by nutritional or targeted therapeutic interventions during the period of developmental plasticity. This review will discuss critical windows of developmental plasticity and possible avenues to ameliorate the development of postnatal metabolic disorders following an adverse early life environment.

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“…Chromium is an essential trace mineral recognized for increasing insulin function and insulin sensitivity not only in humans and laboratory rodents (Vincent, 2000;Anderson, 2003;Padmavathi et al, 2010) but also in livestock (Kegley et al, 1997b;Sumner et al, 2007;Spears et al, 2012). Supplementing Cr to heifers approximately 1 yr old increased insulin sensitivity (Sumner et al, 2007;Spears et al, 2012) but decreased insulin sensitivity in beef feeder calves during the receiving period (Kegley et al, 2000;Bernhard et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Effects of chromium supplementation to feedlot steers on growth performance, insulin sensitivity, and carcass characteristics1

Kneeskern

Dilger

Loerch

et al. 2016

Journal of Animal Science

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Objectives were to determine the effects of chromium propionate supplementation on growth performance, insulin and glucose metabolism, and carcass characteristics of beef cattle. Steers ( = 34) were stratified by BW and assigned to 1 of 2 treatments: 1) no supplemental Cr (Cont) or 2) 3 mg supplemental Cr·steer·d (CrP). Both supplements, Cont and CrP, were delivered via 0.454 kg ground corn top-dressed on the basal diet. There was no effect ( ≥ 0.45) of CrP on ADG, DMI, G:F, or final BW. However, steers fed CrP needed more ( = 0.10) days on feed (DOF) to achieve the same carcass back fat (BF) as steers fed Cont. There were no effects ( ≥ 0.41) of CrP on HCW, BF, or KPH. Steers fed CrP had increased ( = 0.01) dressing percentage (DP) and tended to have a 4.21 cm greater LM area ( = 0.15), decreased marbling scores ( = 0.11), and decreased intramuscular fat ( = 0.11) compared to steers fed Cont. There were no differences ( ≥ 0.25) in quality or yield grade distributions. A glucose tolerance test was conducted early (21 DOF) and late (98 DOF) in the finishing phase. There was a feedlot treatment (FT) × time × DOF interaction ( = 0.08) for glucose concentrations, but no other interactions ( ≥ 0.21) for glucose or insulin concentrations. There were no FT × DOF interactions ( ≥ 0.21) for insulin area under the curve (iAUC), insulin:glucose ratio, insulin or glucose baseline, or peak insulin or glucose concentrations. At 21 DOF, steers fed CrP had decreased glucose area under the curve (gAUC; = 0.01), decreased glucose clearance rate (; = 0.02), and increased glucose half-life (T; = 0.07) compared to steers fed Cont; however, by 98 DOF, no differences were observed between treatments. At 98 DOF, all steers, regardless of treatment, had increased ( < 0.01) peak glucose and insulin, , iAUC, insulin:glucose ratio, and baseline insulin when compared to values at 21 DOF, but gAUC and T decreased ( < 0.01). Although steers fed CrP tended ( = 0.11) to have increased baseline glucose concentrations compared to steers fed Cont, CrP supplementation did not affect ( ≥ 0.17) other measures of glucose or insulin. Results of this study indicate that CrP increased DP and tended to increase LM area but tended to decrease intramuscular fat, with no effect on growth performance. With increased DOF, all steers became more insulin resistant, using more insulin to clear less glucose, and these effects were not mitigated by CrP supplementation.

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Maternal dietary chromium restriction programs muscle development and function in the rat offspring

Cited by 14 publications

References 46 publications

Impact of maternal chromium restriction on glucose tolerance, plasma insulin and oxidative stress in WNIN rat offspring

Impact of maternal chromium restriction on glucose tolerance, plasma insulin and oxidative stress in WNIN rat offspring

Developmental programming of the metabolic syndrome - critical windows for intervention

Effects of chromium supplementation to feedlot steers on growth performance, insulin sensitivity, and carcass characteristics1

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