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ros-reactive-oxygen-species

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Unified mechanism for NAC effects on HFD dams that program the metabolic he...
Published: 22 May 2020
Figure 6 Unified mechanism for NAC effects on HFD dams that program the metabolic health of offspring. ROS, reactive oxygen species. Figure 6. Unified mechanism for NAC effects on HFD dams that program the metabolic health of offspring. ROS, reactive oxygen species. More
Meeting Abstracts
Journal: Diabetes
Diabetes 2018;67(Supplement_1):1857-P
Published: 01 July 2018
... of 5.5 mM fructose or 0.5 mM palmitate. Addition of fructose or palmitate induced lipid accumulation in cells on 500 Pa gels and increased ROS (reactive oxygen species) accumulation in hepatocytes on 500 Pa PAA gels, but not in hepatocytes on glass. Fructose or palmitate treatment also caused HMGB1 (High...
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In diabetic nephropathy, hyperglycemia initiates various intracellular sign...
Published: 14 March 2013
FIG. 1. In diabetic nephropathy, hyperglycemia initiates various intracellular signaling pathways resulting in further downstream activation of different PKC isoforms. ROS, reactive oxygen species; CTGF, connective tissue growth factor. FIG. 1. In diabetic nephropathy, hyperglycemia initiates va... More
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Models illustrating the influence of calorigenic nutrients and overnutritio...
Published: 01 December 2002
FIG. 1. Models illustrating the influence of calorigenic nutrients and overnutrition in the etiology of adipogenic type 2 diabetes (A) and type 1 diabetes (B). CNS, central nervous system; ROS, reactive oxygen species. FIG. 1. Models illustrating the influence of calorigenic nutrients and overnutrition in the etiology of adipogenic type 2 diabetes (A) and type 1 diabetes (B). CNS, central nervous system; ROS, reactive oxygen species. More
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Models illustrating the influence of calorigenic nutrients and overnutritio...
Published: 01 December 2002
FIG. 1. Models illustrating the influence of calorigenic nutrients and overnutrition in the etiology of adipogenic type 2 diabetes (A) and type 1 diabetes (B). CNS, central nervous system; ROS, reactive oxygen species. FIG. 1. Models illustrating the influence of calorigenic nutrients and overnutrition in the etiology of adipogenic type 2 diabetes (A) and type 1 diabetes (B). CNS, central nervous system; ROS, reactive oxygen species. More
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GLP-1R agonists and endothelial function. Potential signaling pathways in e...
Published: 17 June 2015
Figure 1 GLP-1R agonists and endothelial function. Potential signaling pathways in endothelial and nonendothelial cells and tissues responsible for the effects of GLP-1R agonists on improving endothelial function are shown. Hashed lines represent potential pathways; solid lines represent known pat... More
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Schematic overview summarizing our proposed model for the molecular mechani...
Published: 22 March 2011
FIG. 6. Schematic overview summarizing our proposed model for the molecular mechanisms initiated by the activation of the ghrelin receptor leading to AMPK activation and finally to an increased feeding behavior. ROS, reactive oxygen species; CPT, carnitine palmitoyltransferase; UCP, uncoupling pro... More
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Schematic representation of TXNIP deficiency-mediated protection against β-...
Published: 29 October 2009
FIG. 6. Schematic representation of TXNIP deficiency-mediated protection against β-cell apoptosis. Excess glucose (GLUC) or fatty acids (FA) ultimately lead to β-cell apoptosis by mitochondrial (staurosporine-induced) or ER stress (thapsigargin-induced) pathways. Despite extensive cross talk, TXNI... More
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The three nutrient-sensing pathways, mTOR, AMPK, and SIRT1, may be independ...
Published: 12 December 2011
FIG. 2. The three nutrient-sensing pathways, mTOR, AMPK, and SIRT1, may be independently and coordinately involved in the pathogenesis of diabetic nephropathy. 4E-BP, 4E-binding protein; COX2, cyclooxygenase-2; eNOS, endothelial nitric oxide synthase; EPO, erythropoietin; FoxO, forkhead box class ... More
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Proposed effects of EXOs released by islet MSCs. Although there is the poss...
Published: 13 February 2014
Figure 1 Proposed effects of EXOs released by islet MSCs. Although there is the possibility that EXOs directly stimulate T and B cells, it is likely that EXOs affect DCs that, in turn, initiate anti-β-cell–specific T-cell response. EXOs may lead to the maturation of inflammatory DCs or “feed” DCs ... More
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Schematic diagram depicting the metabolism of heme and the beneficial actio...
Published: 16 April 2015
Figure 1 Schematic diagram depicting the metabolism of heme and the beneficial actions of bilirubin in diabetes-induced endothelial dysfunction. Bilirubin, generated by the concerted action of HO-1 and BVR, leads to the sequential activation of Akt and eNOS and synthesis of NO, which improves endothelium-dependent vasodilation and insulin resistance. These salutary actions are further amplified by the ability of bilirubin to inhibit PKC, inflammation, and oxidative stress, which are known mediators of endothelial dysfunction in diabetes. Bilirubin is removed from the circulation by the liver and metabolized by UGT1A1 to yield water-soluble conjugated bilirubin for elimination. BR, bilirubin; BV, biliverdin; Fe2+, ferrous iron; ROS, reactive oxygen species. Figure 1. Schematic diagram depicting the metabolism of heme and the beneficial actions of bilirubin in diabetes-induced endothelial dysfunction. Bilirubin, generated by the concerted action of HO-1 and BVR, leads to the sequential activation of Akt and eNOS and synthesis of NO, which improves endothelium-dependent vasodilation and insulin resistance. These salutary actions are further amplified by the ability of bilirubin to inhibit PKC, inflammation, and oxidative stress, which are known mediators of endothelial dysfunction in diabetes. Bilirubin is removed from the circulation by the liver and metabolized by UGT1A1 to yield water-soluble conjugated bilirubin for elimination. BR, bilirubin; BV, biliverdin; Fe2+, ferrous iron; ROS, reactive oxygen species. More
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Selective insulin resistance in vascular ECs. Selective insulin resistance ...
Published: 18 May 2016
Figure 3 Selective insulin resistance in vascular ECs. Selective insulin resistance in ECs occurs when angiotensin II, elevated FFA and glucose levels, and proinflammatory cytokines induced by diabetes and insulin resistance stimulate PKC isoforms and other stress kinases to phosphorylate IRS1/2 a... More
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Schematic representation of the complex regulation of gluconeogenesis by ch...
Published: 17 March 2015
Figure 1 Schematic representation of the complex regulation of gluconeogenesis by changes in dietary iron and the self-regulated feedback loops that rigorously control the pathway. PGC-1α and AMPK are critical regulators of gluconeogenesis in the liver. As shown, dietary iron can suppress gluconeo... More
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Hypothesized mechanisms of air pollution–mediated cardiometabolic disease w...
Published: 15 November 2012
FIG. 2. Hypothesized mechanisms of air pollution–mediated cardiometabolic disease wherein inhalational or nutritional signals either directly or via the generation of signals such as DAMPs may serve to activate innate immune mechanisms such as the TLR and NLR. AP1, activator protein 1; CARD, caspa... More
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ECSHIP2<sup>Δ/+</sup> ECs exhibit PI3K- and Nox2-dependent oxidative stress...
Published: 22 August 2017
Figure 6 ECSHIP2Δ/+ ECs exhibit PI3K- and Nox2-dependent oxidative stress and reduced NO generation. A: Increased superoxide generation in ECSHIP2Δ/+ mice, measured with lucigenin-enhanced chemiluminescence (left: n ≥10) and dihydroethidium (DHE) fluorescence (right: n ≥3). B: Increased Nox2 NADPH oxidase protein (representative Western blot shown above the panel) in ECSHIP2Δ/+ mice (n ≥9). C: Increased superoxide abundance in ECSHIP2Δ/+ mice is normalized by Gp91ds-tat (n ≥4). D: Increased superoxide abundance in ECSHIP2Δ/+ mice is normalized by the PI3K inhibitors Wortmannin and LY294002 (n ≥4). E: Insulin-stimulated NO production is impaired in ECs from ECSHIP2Δ/+ mice (n ≥5). ROS, reactive oxygen species. AU, arbitrary units; GP-tat, Gp91ds-tat NADPH oxidase 2 inhibitor; WT, Wortmannin; LY, LY294002 PI3K inhibitor. *P < 0.05. Figure 6. ECSHIP2Δ/+ ECs exhibit PI3K- and Nox2-dependent oxidative stress and reduced NO generation. A: Increased superoxide generation in ECSHIP2Δ/+ mice, measured with lucigenin-enhanced chemiluminescence (left: n ≥10) and dihydroethidium (DHE) fluorescence (right: n ≥3). B: Increased Nox2 NADPH oxidase protein (representative Western blot shown above the panel) in ECSHIP2Δ/+ mice (n ≥9). C: Increased superoxide abundance in ECSHIP2Δ/+ mice is normalized by Gp91ds-tat (n ≥4). D: Increased superoxide abundance in ECSHIP2Δ/+ mice is normalized by the PI3K inhibitors Wortmannin and LY294002 (n ≥4). E: Insulin-stimulated NO production is impaired in ECs from ECSHIP2Δ/+ mice (n ≥5). ROS, reactive oxygen species. AU, arbitrary units; GP-tat, Gp91ds-tat NADPH oxidase 2 inhibitor; WT, Wortmannin; LY, LY294002 PI3K inhibitor. *P < 0.05. More
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Mg<sup>2+</sup> affects insulin sensitivity. Mg<sup>2+</sup> regulates the ...
Published: 16 December 2015
Figure 1 Mg2+ affects insulin sensitivity. Mg2+ regulates the insulin signaling pathway by increasing the affinity of the insulin receptor tyrosine kinase for ATP. Consequently, hypomagnesemia is associated with a reduced activity of all downstream pathways. In the muscle, Mg2+ therefore regulates the membrane trafficking of GLUT4. In the liver, Mg2+ is an important regulator of enzymes in gluconeogenesis, including G6Pase and PEPCK. In adipose tissue, Mg2+ acts as an anti-inflammatory factor reducing IL-1 and TNF-α secretion. FOXO1, forkhead box class O1; Grb2, growth factor receptor-bound protein 2; GSK3, glycogen synthase kinase 3; MEK/MAPK, mitogen-activated protein kinase kinase; P, phosphorylation; PIP3, phosphatidylinositol 3,4,5 trisphosphate; PI3K, phosphatidylinositol 3-kinase; PKC, protein kinase C; ROS, reactive oxygen species; Shc, Src homology 2 domain containing transforming protein. Figure 1. Mg2+ affects insulin sensitivity. Mg2+ regulates the insulin signaling pathway by increasing the affinity of the insulin receptor tyrosine kinase for ATP. Consequently, hypomagnesemia is associated with a reduced activity of all downstream pathways. In the muscle, Mg2+ therefore regulates the membrane trafficking of GLUT4. In the liver, Mg2+ is an important regulator of enzymes in gluconeogenesis, including G6Pase and PEPCK. In adipose tissue, Mg2+ acts as an anti-inflammatory factor reducing IL-1 and TNF-α secretion. FOXO1, forkhead box class O1; Grb2, growth factor receptor-bound protein 2; GSK3, glycogen synthase kinase 3; MEK/MAPK, mitogen-activated protein kinase kinase; P, phosphorylation; PIP3, phosphatidylinositol 3,4,5 trisphosphate; PI3K, phosphatidylinositol 3-kinase; PKC, protein kinase C; ROS, reactive oxygen species; Shc, Src homology 2 domain containing transforming protein. More
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Mechanisms of action for the NO<sub>2</sub><sup>−</sup> in cardiovascular d...
Published: 13 December 2013
Figure 1 Mechanisms of action for the NO2 in cardiovascular diseases. Under normal conditions, NO2 is fairly stable and available from conventional L-arginine/NOS pathway, NO2 therapy, and dietary consumption of NO3/NO2 leading to salivary NO3 secretion and reduction to NO2 by commensal bacteria. However, during ischemia, low pH, and hypoxia, NO2 is reduced to NO via deoxyhemoglobin, deoxymyoglobin, xanthine oxidoreductase, myoglobin, and aldehyde oxidase. NO induces EC migration, proliferation, and angiogenesis by activating cGMP/PKG, Ras-Raf, and MAPK signaling pathways. NO activates HIF-1 and heme oxygenase 1 pathways to increase VEGF production, which can increase NO in turn by upregulating eNOS activity. NO2 therapy confers substantial benefit to cardiovascular disease. cGMP, cyclic guanosine monophosphate; HIF-1, hypoxia-inducible factor 1; MAPK, mitogen-activated protein kinases; NO3, nitrate; NO2, nitrite; PKG, protein kinase G; RBC, red blood cell; ROS, reactive oxygen species; sGC, solube guanylate cyclase. Figure 1. Mechanisms of action for the NO2− in cardiovascular diseases. Under normal conditions, NO2− is fairly stable and available from conventional L-arginine/NOS pathway, NO2− therapy, and dietary consumption of NO3−/NO2− leading to salivary NO3− secretion and reduction to NO2− by commensal bacteria. However, during ischemia, low pH, and hypoxia, NO2− is reduced to NO via deoxyhemoglobin, deoxymyoglobin, xanthine oxidoreductase, myoglobin, and aldehyde oxidase. NO induces EC migration, proliferation, and angiogenesis by activating cGMP/PKG, Ras-Raf, and MAPK signaling pathways. NO activates HIF-1 and heme oxygenase 1 pathways to increase VEGF production, which can increase NO in turn by upregulating eNOS activity. NO2− therapy confers substantial benefit to cardiovascular disease. cGMP, cyclic guanosine monophosphate; HIF-1, hypoxia-inducible factor 1; MAPK, mitogen-activated protein kinases; NO3−, nitrate; NO2−, nitrite; PKG, protein kinase G; RBC, red blood cell; ROS, reactive oxygen species; sGC, solube guanylate cyclase. More
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shRNA knockdown of SHIP2 in HUVECs recapitulates the phenotype of ECSHIP2...
Published: 22 August 2017
Figure 7 shRNA knockdown of SHIP2 in HUVECs recapitulates the phenotype of ECSHIP2Δ/+ ECs. A: SHIP2 shRNA reduced SHIP2 protein by ∼75% vs. control shRNA (n = 3; representative Western blot shown above the panel). B: SHIP2 activity is reduced by SHIP2 shRNA (n = 3). C: Increased superoxide abundance in SHIP2 knockdown HUVECs measured by lucigenin-enhanced chemiluminescence (n = 3). D: Increased Nox2 NADPH oxidase protein in SHIP2 knockdown HUVECs (n = 5; representative Western blot shown above the panel). Suppression of excess superoxide production in SHIP2 knockdown HUVECs by the NOX2 inhibitor Gp91ds-tat, which was measured with lucigenin-enhanced chemiluminescence (n ≥3) (E) and dihydroethidium (DHE) fluorescence (n = 6) (F). G: Increased concentration of S473 pAkt and S1177 peNOS in SHIP2 knockdown HUVECs (n = 5). H: Suppression of excess superoxide production in SHIP2 knockdown HUVECs by the PI3K inhibitors Wortmannin and LY294002 (n = 5). AU, arbitrary units; ROS, reactive oxygen species; GP-tat, Gp91ds-tat NADPH oxidase 2 inhibitor; WT, Wortmannin; LY, LY294002 PI3K inhibitor. *P < 0.05. Figure 7. shRNA knockdown of SHIP2 in HUVECs recapitulates the phenotype of ECSHIP2Δ/+ ECs. A: SHIP2 shRNA reduced SHIP2 protein by ∼75% vs. control shRNA (n = 3; representative Western blot shown above the panel). B: SHIP2 activity is reduced by SHIP2 shRNA (n = 3). C: Increased superoxide abundance in SHIP2 knockdown HUVECs measured by lucigenin-enhanced chemiluminescence (n = 3). D: Increased Nox2 NADPH oxidase protein in SHIP2 knockdown HUVECs (n = 5; representative Western blot shown above the panel). Suppression of excess superoxide production in SHIP2 knockdown HUVECs by the NOX2 inhibitor Gp91ds-tat, which was measured with lucigenin-enhanced chemiluminescence (n ≥3) (E) and dihydroethidium (DHE) fluorescence (n = 6) (F). G: Increased concentration of S473 pAkt and S1177 peNOS in SHIP2 knockdown HUVECs (n = 5). H: Suppression of excess superoxide production in SHIP2 knockdown HUVECs by the PI3K inhibitors Wortmannin and LY294002 (n = 5). AU, arbitrary units; ROS, reactive oxygen species; GP-tat, Gp91ds-tat NADPH oxidase 2 inhibitor; WT, Wortmannin; LY, LY294002 PI3K inhibitor. *P < 0.05. More
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Habitual dietary SFA, but not MUFA, promotes IR. <em>A–C</em>: T2D ...
Published: 27 January 2015
Figure 7 Habitual dietary SFA, but not MUFA, promotes IR. A–C: T2D subjects from the CORDIOPREV study (NCT00924937) were categorized based on tertiles of baseline fasting plasma SFA and MUFA concentrations. A: ISI is represented according to SFA and MUFA tertiles. B: HOMA-IR is represented according to SFA and MUFA tertiles. C: C-reactive protein is represented according to SFA tertiles. Black bars, SFA. In A–C: **P < 0.01, w.r.t. tertile 1; #P < 0.05, w.r.t tertile 2; n = 160–184. D: Schematic representation illustrating the differential effects of an SFA-HFD vs. a MUFA-HFD on pro-IL-1β priming and NLRP3 inflammasome activation: 1, MUFA-HFD lacks the ability to prime pro-IL-1β in SVF; 2, MUFA-HFD maintains adipose protein pAMPK levels at those of chow-fed mice, while SFA-HFD–fed mice display reduced pAMPK levels; 3, caspase-1 activity is significantly increased in BMMs from SFA-HFD–fed mice; 4, greater levels of IL-1β are secreted from SFA SVF compared with MUFA SVF; 5, protein pAKT levels are reduced in SFA adipose tissue compared with MUFA adipose tissue; and 6, a MUFA-HFD induced a hyperplastic adipose morphology, while an SFA-HFD induced adipocyte hypertrophy. NFκB, nuclear factor-κB; ROS, reactive oxygen species. Figure 7. Habitual dietary SFA, but not MUFA, promotes IR. A–C: T2D subjects from the CORDIOPREV study (NCT00924937) were categorized based on tertiles of baseline fasting plasma SFA and MUFA concentrations. A: ISI is represented according to SFA and MUFA tertiles. B: HOMA-IR is represented according to SFA and MUFA tertiles. C: C-reactive protein is represented according to SFA tertiles. Black bars, SFA. In A–C: **P < 0.01, w.r.t. tertile 1; #P < 0.05, w.r.t tertile 2; n = 160–184. D: Schematic representation illustrating the differential effects of an SFA-HFD vs. a MUFA-HFD on pro-IL-1β priming and NLRP3 inflammasome activation: 1, MUFA-HFD lacks the ability to prime pro-IL-1β in SVF; 2, MUFA-HFD maintains adipose protein pAMPK levels at those of chow-fed mice, while SFA-HFD–fed mice display reduced pAMPK levels; 3, caspase-1 activity is significantly increased in BMMs from SFA-HFD–fed mice; 4, greater levels of IL-1β are secreted from SFA SVF compared with MUFA SVF; 5, protein pAKT levels are reduced in SFA adipose tissue compared with MUFA adipose tissue; and 6, a MUFA-HFD induced a hyperplastic adipose morphology, while an SFA-HFD induced adipocyte hypertrophy. NFκB, nuclear factor-κB; ROS, reactive oxygen species. More
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Programmed effects in the liver and bone marrow immune cells of NHP offspri...
Published: 11 October 2018
Figure 1 Programmed effects in the liver and bone marrow immune cells of NHP offspring exposed to maternal WSD. A: Livers from fetal offspring (early third trimester) of obese, WSD-fed NHP dams demonstrate increases in gluconeogenic genes, oxidative stress, and triglyceride accumulation. Diet reversal in obese mothers produces fetuses with lower lipogenic gene expression and normalized oxidative stress yet persistently higher triglycerides, demonstrating incomplete amelioration of the steatotic phenotype. Global metabolomic profiling of fetal liver and serum revealed decreased tricarboxylic acid (TCA) cycle intermediates, increased amino acid metabolism, and increased gluconeogenesis, indicating increased reliance on amino acid metabolism to meet energy needs in fetuses from obese, WSD-fed mothers. These fetuses have lower arterial oxygenation suggestive of mild hypoxia and exposure to higher plasma cytokine levels (shown in green). Incomplete mitochondrial and lipid oxidation and/or respiratory chain dysfunction, when combined with limited antioxidant activity, increases hepatic oxidative stress and liver injury prior to the development of obesity. Juvenile offspring from WSD-fed dams show innate immune (Kupffer cell) activation and inflammatory cytokine expression (interleukin-6 [IL-6], tumor necrosis factor-α [TNFα]) and a persistent increase in lipogenic gene expression (fatty acid synthase [FAS], sterol regulatory element binding protein [SREBP], acetyl-CoA carboxylase [ACC]) in vivo and in vitro (shown in red), even after weaning to a chow diet. B: Maternal WSD persistently alters bone marrow immune cell proportions in NHP offspring. Bone marrow from 3-year-old juvenile offspring exposed to maternal WSD, then shifted to a chow diet (CON) at weaning, was studied using colony-forming assays of plated bone marrow cells. A significant 34.5% (P < 0.05) relative increase in myeloid cell proliferation was observed at the expense of erythroid (−78.9%) and multilineage (−53.8%) progenitor cell types. RBCs, red blood cells; ROS, reactive oxygen species; WBCs, white blood cells. Figure 1. Programmed effects in the liver and bone marrow immune cells of NHP offspring exposed to maternal WSD. A: Livers from fetal offspring (early third trimester) of obese, WSD-fed NHP dams demonstrate increases in gluconeogenic genes, oxidative stress, and triglyceride accumulation. Diet reversal in obese mothers produces fetuses with lower lipogenic gene expression and normalized oxidative stress yet persistently higher triglycerides, demonstrating incomplete amelioration of the steatotic phenotype. Global metabolomic profiling of fetal liver and serum revealed decreased tricarboxylic acid (TCA) cycle intermediates, increased amino acid metabolism, and increased gluconeogenesis, indicating increased reliance on amino acid metabolism to meet energy needs in fetuses from obese, WSD-fed mothers. These fetuses have lower arterial oxygenation suggestive of mild hypoxia and exposure to higher plasma cytokine levels (shown in green). Incomplete mitochondrial and lipid oxidation and/or respiratory chain dysfunction, when combined with limited antioxidant activity, increases hepatic oxidative stress and liver injury prior to the development of obesity. Juvenile offspring from WSD-fed dams show innate immune (Kupffer cell) activation and inflammatory cytokine expression (interleukin-6 [IL-6], tumor necrosis factor-α [TNFα]) and a persistent increase in lipogenic gene expression (fatty acid synthase [FAS], sterol regulatory element binding protein [SREBP], acetyl-CoA carboxylase [ACC]) in vivo and in vitro (shown in red), even after weaning to a chow diet. B: Maternal WSD persistently alters bone marrow immune cell proportions in NHP offspring. Bone marrow from 3-year-old juvenile offspring exposed to maternal WSD, then shifted to a chow diet (CON) at weaning, was studied using colony-forming assays of plated bone marrow cells. A significant 34.5% (P < 0.05) relative increase in myeloid cell proliferation was observed at the expense of erythroid (−78.9%) and multilineage (−53.8%) progenitor cell types. RBCs, red blood cells; ROS, reactive oxygen species; WBCs, white blood cells. More