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Special Issue "Nutritional Control of Metabolism"

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (25 January 2014)

Special Issue Editors

Guest Editor
Prof. Dr. J. Alfredo Martínez Hernández

Department of Nutrition, Food Sciences and Physiology, University of Navarra, Pamplona 31008, Spain
Website | E-Mail
Interests: nutritional control of metabolism; the nutritional utilization of functional foods; the evaluation of nutritional status in different populations; nutrition and inflammation; and cell, animal and human .experimental. interventional and epidemiological studies in obesity
Guest Editor
Dr. Pedro Gonzalez-Muniesa

Department of Nutrition, Food Sciences and Physiology. University of Navarra, Pamplona 31008, Spain
Website | E-Mail
Interests: UCPs (uncoupling proteins), gene therapy, ANGPTL4, endocannabinoid system, antioxidant defenses and mitochondria, stress, inflammation, obesity and adipose tissue; and specifically the relation of oxygen with inflammation and weight.

Special Issue Information

Dear Colleagues,

Nutrients provide substrates, energy and specific regulatory elements influencing all metabolic pathways in the organism. Cell structures and functions are strictly regulated by different mechanisms, where nutritional factors, food components as well as a number of endogenous and environmental factors have an impact. Genetically and phenotypically molecular dependent processes involving biochemical reactions, hormones and endocrine mediators, enzymes, transcription factors, etc are affected by feeding and fasting.

In this context, the aim of this issue of the International Journal of Molecular Sciences is specifically focused in providing novel concepts and updated critical views about the nutritional control of metabolism considering some of the following scopes and scientific perspectives, but not limited to:

Role of dietary carbohydrates/fibre on glucose metabolism;
Role of specific amino acids on energy homeostasis;
Omega 3 and other fatty acids and inflammation;
New roles of Vitamins in regulating metabolic disturbances;

Antioxidants and mitochondrial functions;
Vitamin D and metabolic syndrome features;
Genetic programming associated to perinatal nutrition;

Endocrine control of nutritional pathways: New hormones and adipokines;
Chrononutrition and nutrient metabolism;
Nutritional control of the oxidative status;
Nutrigenetics and nutrigenomics aspects of the nutritional control of metabolism;
Role of Hypoxia and Hyperoxia on cell metabolism.

Prof. Dr. J. Alfredo Martínez Hernández
Dr. Pedro González-Muniesa
Guest Editors

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed Open Access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF.


Keywords

  • nutrigenetics
  • nutrigenomics
  • chrononutrition
  • oxidative status
  • hypoxia and hyperoxia
  • hormones and adipokines
  • perinatal nutrition
  • antioxidants
  • omega 3
  • carbohydrates/fibre
  • vitamins
  • amino acids

Published Papers (13 papers)

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Research

Jump to: Review, Other

Open AccessArticle Mangiferin Facilitates Islet Regeneration and β-Cell Proliferation through Upregulation of Cell Cycle and β-Cell Regeneration Regulators
Int. J. Mol. Sci. 2014, 15(5), 9016-9035; doi:10.3390/ijms15059016
Received: 16 January 2014 / Revised: 21 April 2014 / Accepted: 24 April 2014 / Published: 20 May 2014
Cited by 7 | PDF Full-text (3835 KB) | HTML Full-text | XML Full-text
Abstract
Mangiferin, a xanthonoid found in plants including mangoes and iris unguicularis, was suggested in previous studies to have anti-hyperglycemic function, though the underlying mechanisms are largely unknown. This study was designed to determine the therapeutic effect of mangiferin by the regeneration of β-cells
[...] Read more.
Mangiferin, a xanthonoid found in plants including mangoes and iris unguicularis, was suggested in previous studies to have anti-hyperglycemic function, though the underlying mechanisms are largely unknown. This study was designed to determine the therapeutic effect of mangiferin by the regeneration of β-cells in mice following 70% partial pancreatectomy (PPx), and to explore the mechanisms of mangiferin-induced β-cell proliferation. For this purpose, adult C57BL/6J mice after 7–14 days post-PPx, or a sham operation were subjected to mangiferin (30 and 90 mg/kg body weight) or control solvent injection. Mangiferin-treated mice exhibited an improved glycemia and glucose tolerance, increased serum insulin levels, enhanced β-cell hyperplasia, elevated β-cell proliferation and reduced β-cell apoptosis. Further dissection at the molecular level showed several key regulators of cell cycle, such as cyclin D1, D2 and cyclin-dependent kinase 4 (Cdk4) were significantly up-regulated in mangiferin-treated mice. In addition, critical genes related to β-cell regeneration, such as pancreatic and duodenal homeobox 1 (PDX-1), neurogenin 3 (Ngn3), glucose transporter 2 (GLUT-2), Forkhead box protein O1 (Foxo-1), and glucokinase (GCK), were found to be promoted by mangiferin at both the mRNA and protein expression level. Thus, mangiferin administration markedly facilitates β-cell proliferation and islet regeneration, likely by regulating essential genes in the cell cycle and the process of islet regeneration. These effects therefore suggest that mangiferin bears a therapeutic potential in preventing and/or treating the diabetes. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Open AccessArticle Influence of Diet, Menstruation and Genetic Factors on Iron Status: A Cross-Sectional Study in Spanish Women of Childbearing Age
Int. J. Mol. Sci. 2014, 15(3), 4077-4087; doi:10.3390/ijms15034077
Received: 24 January 2014 / Revised: 26 February 2014 / Accepted: 27 February 2014 / Published: 6 March 2014
Cited by 9 | PDF Full-text (203 KB) | HTML Full-text | XML Full-text
Abstract
The aim of this study was to investigate the combined influence of diet, menstruation and genetic factors on iron status in Spanish menstruating women (n = 142). Dietary intake was assessed by a 72-h detailed dietary report and menstrual blood loss by
[...] Read more.
The aim of this study was to investigate the combined influence of diet, menstruation and genetic factors on iron status in Spanish menstruating women (n = 142). Dietary intake was assessed by a 72-h detailed dietary report and menstrual blood loss by a questionnaire, to determine a Menstrual Blood Loss Coefficient (MBLC). Five selected SNPs were genotyped: rs3811647, rs1799852 (Tf gene); rs1375515 (CACNA2D3 gene); and rs1800562 and rs1799945 (HFE gene, mutations C282Y and H63D, respectively). Iron biomarkers were determined and cluster analysis was performed. Differences among clusters in dietary intake, menstrual blood loss parameters and genotype frequencies distribution were studied. A categorical regression was performed to identify factors associated with cluster belonging. Three clusters were identified: women with poor iron status close to developing iron deficiency anemia (Cluster 1, n = 26); women with mild iron deficiency (Cluster 2, n = 59) and women with normal iron status (Cluster 3, n = 57). Three independent factors, red meat consumption, MBLC and mutation C282Y, were included in the model that better explained cluster belonging (R2 = 0.142, p < 0.001). In conclusion, the combination of high red meat consumption, low menstrual blood loss and the HFE C282Y mutation may protect from iron deficiency in women of childbearing age. These findings could be useful to implement adequate strategies to prevent iron deficiency anemia. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Open AccessArticle Inhibition of Aflatoxin Synthesis in Aspergillus flavus by Three Structurally Modified Lentinans
Int. J. Mol. Sci. 2014, 15(3), 3860-3870; doi:10.3390/ijms15033860
Received: 31 December 2013 / Revised: 20 February 2014 / Accepted: 20 February 2014 / Published: 4 March 2014
Cited by 4 | PDF Full-text (655 KB) | HTML Full-text | XML Full-text
Abstract
The chemical properties of β-glucans leading to their inhibition on aflatoxin (AF) production by Aspergillus flavus remain unclear. In this study, structurally modified lentinan derivatives were prepared by carboxymethylation, sulfation, and phosphorylation to explore their inhibition activity to AF synthesis. The results demonstrated
[...] Read more.
The chemical properties of β-glucans leading to their inhibition on aflatoxin (AF) production by Aspergillus flavus remain unclear. In this study, structurally modified lentinan derivatives were prepared by carboxymethylation, sulfation, and phosphorylation to explore their inhibition activity to AF synthesis. The results demonstrated that inhibitory activity of lentinan decreased at higher or lower concentrations than 200 μg/mL. Compared with lentinan, the sulphated derivatives only performed a reduced optimal inhibition rate at a higher concentration. The phosphorylated derivatives achieved complete inhibition of AF production at 50 μg/mL, but the inhibitory activity was attenuated with an increase of concentration. The minimum concentration of carboxymethylated derivatives to completely inhibit AF synthesis was the same as that of the original lentinan, whereas their inhibition activity was not reduced at the increasing concentration. RT-PCR analyses were conducted to understand the effects of lentinan and its carboxymethylated derivatives on the transcription of certain genes associated with AF biosynthesis. The results showed that lentinan delayed the transcription of aflQ, whereas its carboxymethylated derivatives promoted the transcriptions of all the tested genes. Our results revealed that some chemical group features apart from the β-bond could play the vital role in the prevention of AF formation by polysaccharide, and highlighted the structural modifications which could promote its practicability in the control of aflatoxin contamination. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Open AccessArticle Lipidomic Analysis of Serum from High Fat Diet Induced Obese Mice
Int. J. Mol. Sci. 2014, 15(2), 2991-3002; doi:10.3390/ijms15022991
Received: 17 December 2013 / Revised: 22 January 2014 / Accepted: 11 February 2014 / Published: 20 February 2014
Cited by 16 | PDF Full-text (359 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Lipid metabolites regulate fatty acid and glucose homeostasis. The intention of the current study is to identify circulating lipid species, which are altered in rodent obesity and strongly correlate with the classically measured metabolites glucose, triglycerides, and cholesterol. Mice fed a high fat
[...] Read more.
Lipid metabolites regulate fatty acid and glucose homeostasis. The intention of the current study is to identify circulating lipid species, which are altered in rodent obesity and strongly correlate with the classically measured metabolites glucose, triglycerides, and cholesterol. Mice fed a high fat diet (HFD) for 14 weeks have increased body weight and fasting glucose. Serum triglycerides are not altered, while cholesterol tends to be increased. Accordingly, major cholesteryl ester (CE) species and free cholesterol are not significantly raised in obesity while minor metabolites, including CE 20:3 and CE 18:3, are increased or reduced, respectively. Distinct sphingomyelin (SM) species are elevated while ceramides are not raised. Phosphatidylinositol (PI) species, including PI 34:1, are raised while others are decreased. PI 34:1 strongly correlates with fasting glucose and proinsulin levels. Phosphatidylcholine (PC) 26:0, 40:2, and 40:5, which are induced in obesity, correlate with cholesterol. PC 38:4 and PC 40:6 are also raised in fat fed mice and positively correlate with fasting glucose. Lysophosphatidylcholine (LPC) species are also changed in obesity and the already shown reduction of LPC 16:1 has been confirmed. LPC 22:4, which is increased, correlates with serum cholesterol. The data indicate that circulating levels of various lipid species are changed in the obesity model studied and some of them are strongly associated with classically measured metabolites. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Open AccessArticle Differential Effects of High-Fish Oil and High-Lard Diets on Cells and Cytokines Involved in the Inflammatory Process in Rat Insulin-Sensitive Tissues
Int. J. Mol. Sci. 2014, 15(2), 3040-3063; doi:10.3390/ijms15023040
Received: 7 October 2013 / Revised: 10 February 2014 / Accepted: 12 February 2014 / Published: 20 February 2014
Cited by 12 | PDF Full-text (1129 KB) | HTML Full-text | XML Full-text
Abstract
Dietary fat sources may differentially affect the development of inflammation in insulin-sensitive tissues during chronic overfeeding. Considering the anti-inflammatory properties of ω-3 fatty acids, this study aimed to compare the effects of chronic high-fish oil and high-lard diets on obesity-related inflammation by evaluating
[...] Read more.
Dietary fat sources may differentially affect the development of inflammation in insulin-sensitive tissues during chronic overfeeding. Considering the anti-inflammatory properties of ω-3 fatty acids, this study aimed to compare the effects of chronic high-fish oil and high-lard diets on obesity-related inflammation by evaluating serum and tissue adipokine levels and histological features in insulin-sensitive tissues (white adipose tissue, skeletal muscle and liver). As expected, a high-lard diet induced systemic and peripheral inflammation and insulin resistance. Conversely, compared with a high-lard diet, a high-fish oil diet resulted in a lower degree of systemic inflammation and insulin resistance that were associated with a lower adipocyte diameter as well as lower immunoreactivity for transforming growth factor β 1 (TGFβ1) in white adipose tissue. A high-fish oil diet also resulted in a lower ectopic lipid depot, inflammation degree and insulin resistance in the skeletal muscle and liver. Moreover, a high-fish oil diet attenuated hepatic stellate cell activation and fibrogenesis in the liver, as indicated by the smooth muscle α-actin (α-SMA) and TGFβ1 levels. The replacement of lard (saturated fatty acids) with fish oil (ω-3 fatty acids) in chronic high-fat feeding attenuated the development of systemic and tissue inflammation. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Figures

Open AccessArticle Maternal Methyl Donors Supplementation during Lactation Prevents the Hyperhomocysteinemia Induced by a High-Fat-Sucrose Intake by Dams
Int. J. Mol. Sci. 2013, 14(12), 24422-24437; doi:10.3390/ijms141224422
Received: 28 September 2013 / Revised: 3 December 2013 / Accepted: 10 December 2013 / Published: 16 December 2013
Cited by 13 | PDF Full-text (309 KB) | HTML Full-text | XML Full-text
Abstract
Maternal perinatal nutrition may program offspring metabolic features. Epigenetic regulation is one of the candidate mechanisms that may be affected by maternal dietary methyl donors intake as potential controllers of plasma homocysteine levels. Thirty-two Wistar pregnant rats were randomly assigned into four dietary
[...] Read more.
Maternal perinatal nutrition may program offspring metabolic features. Epigenetic regulation is one of the candidate mechanisms that may be affected by maternal dietary methyl donors intake as potential controllers of plasma homocysteine levels. Thirty-two Wistar pregnant rats were randomly assigned into four dietary groups during lactation: control, control supplemented with methyl donors, high-fat-sucrose and high-fat-sucrose supplemented with methyl donors. Physiological outcomes in the offspring were measured, including hepatic mRNA expression and global DNA methylation after weaning. The newborns whose mothers were fed the obesogenic diet were heavier longer and with a higher adiposity and intrahepatic fat content. Interestingly, increased levels of plasma homocysteine induced by the maternal high-fat-sucrose dietary intake were prevented in both sexes by maternal methyl donors supplementation. Total hepatic DNA methylation decreased in females due to maternal methyl donors administration, while Dnmt3a hepatic mRNA levels decreased accompanying the high-fat-sucrose consumption. Furthermore, a negative association between Dnmt3a liver mRNA levels and plasma homocysteine concentrations was found. Maternal high-fat-sucrose diet during lactation could program offspring obesity features, while methyl donors supplementation prevented the onset of high hyperhomocysteinemia. Maternal dietary intake also affected hepatic DNA methylation metabolism, which could be linked with the regulation of the methionine-homocysteine cycle. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Open AccessArticle Galectin-1 Is an Interactive Protein of Selenoprotein M in the Brain
Int. J. Mol. Sci. 2013, 14(11), 22233-22245; doi:10.3390/ijms141122233
Received: 4 September 2013 / Revised: 24 October 2013 / Accepted: 24 October 2013 / Published: 11 November 2013
Cited by 6 | PDF Full-text (2545 KB) | HTML Full-text | XML Full-text
Abstract
Selenium, an essential trace element for human health, mainly exerts its biological function through selenoproteins. Selenoprotein M (SelM) is one of the highly expressed selenoproteins in the brain, but its biological effect and molecular mechanism remain unclear. Thus, the interactive protein of SelM
[...] Read more.
Selenium, an essential trace element for human health, mainly exerts its biological function through selenoproteins. Selenoprotein M (SelM) is one of the highly expressed selenoproteins in the brain, but its biological effect and molecular mechanism remain unclear. Thus, the interactive protein of SelM was investigated in this paper to guide further study. In order to avoid protein translational stop, the selenocysteine-encoding UGA inside the open reading frame of SelM was site-directly changed to the cysteine-encoding UGC to generate the SelM' mutant. Meanwhile, its N terminal transmembrane signal peptide was also cut off. This truncated SelM' was used to screen a human fetal brain cDNA library by the yeast two-hybrid system. A new interactive protein of SelM' was found to be galectin-1 (Gal-1). This protein-protein interaction was further verified by the results of fluorescence resonance energy transfer techniques, glutathione S-transferase pull-down and co-immunoprecipitation assays. As Gal-1 plays important roles in preventing neurodegeneration and promoting neuroprotection in the brain, the interaction between SelM' and Gal-1 displays a new direction for studying the biological function of SelM in the human brain. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Open AccessArticle Adrenergic Metabolic and Hemodynamic Effects of Octopamine in the Liver
Int. J. Mol. Sci. 2013, 14(11), 21858-21872; doi:10.3390/ijms141121858
Received: 21 September 2013 / Revised: 21 October 2013 / Accepted: 22 October 2013 / Published: 5 November 2013
Cited by 3 | PDF Full-text (365 KB) | HTML Full-text | XML Full-text
Abstract
The fruit extracts of Citrus aurantium (bitter orange) are traditionally used as weight-loss products and as appetite suppressants. A component of these extracts is octopamine, which is an adrenergic agent. Weight-loss and adrenergic actions are always related to metabolic changes and this work
[...] Read more.
The fruit extracts of Citrus aurantium (bitter orange) are traditionally used as weight-loss products and as appetite suppressants. A component of these extracts is octopamine, which is an adrenergic agent. Weight-loss and adrenergic actions are always related to metabolic changes and this work was designed to investigate a possible action of octopamine on liver metabolism. The isolated perfused rat liver was used to measure catabolic and anabolic pathways and hemodynamics. Octopamine increased glycogenolysis, glycolysis, oxygen uptake, gluconeogenesis and the portal perfusion pressure. Octopamine also accelerated the oxidation of exogenous fatty acids (octanoate and oleate), as revealed by the increase in 14CO2 production derived from 14C labeled precursors. The changes in glycogenolysis, oxygen uptake and perfusion pressure were almost completely abolished by α1-adrenergic antagonists. The same changes were partly sensitive to the β-adrenergic antagonist propranolol. It can be concluded that octopamine accelerates both catabolic and anabolic processes in the liver via adrenergic stimulation. Acceleration of oxygen uptake under substrate-free perfusion conditions also means acceleration of the oxidation of endogenous fatty acids, which are derived from lipolysis. All these effects are compatible with an overall stimulating effect of octopamine on metabolism, which is compatible with its reported weight-loss effects in experimental animals. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)

Review

Jump to: Research, Other

Open AccessReview Genetics of Oxidative Stress in Obesity
Int. J. Mol. Sci. 2014, 15(2), 3118-3144; doi:10.3390/ijms15023118
Received: 15 January 2014 / Revised: 12 February 2014 / Accepted: 12 February 2014 / Published: 20 February 2014
Cited by 12 | PDF Full-text (852 KB) | HTML Full-text | XML Full-text
Abstract
Obesity is a multifactorial disease characterized by the excessive accumulation of fat in adipose tissue and peripheral organs. Its derived metabolic complications are mediated by the associated oxidative stress, inflammation and hypoxia. Oxidative stress is due to the excessive production of reactive oxygen
[...] Read more.
Obesity is a multifactorial disease characterized by the excessive accumulation of fat in adipose tissue and peripheral organs. Its derived metabolic complications are mediated by the associated oxidative stress, inflammation and hypoxia. Oxidative stress is due to the excessive production of reactive oxygen species or diminished antioxidant defenses. Genetic variants, such as single nucleotide polymorphisms in antioxidant defense system genes, could alter the efficacy of these enzymes and, ultimately, the risk of obesity; thus, studies investigating the role of genetic variations in genes related to oxidative stress could be useful for better understanding the etiology of obesity and its metabolic complications. The lack of existing literature reviews in this field encouraged us to gather the findings from studies focusing on the impact of single nucleotide polymorphisms in antioxidant enzymes, oxidative stress-producing systems and transcription factor genes concerning their association with obesity risk and its phenotypes. In the future, the characterization of these single nucleotide polymorphisms (SNPs) in obese patients could contribute to the development of controlled antioxidant therapies potentially beneficial for the treatment of obesity-derived metabolic complications. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Open AccessReview Beyond the Role of Dietary Protein and Amino Acids in the Prevention of Diet-Induced Obesity
Int. J. Mol. Sci. 2014, 15(1), 1374-1391; doi:10.3390/ijms15011374
Received: 11 November 2013 / Revised: 9 January 2014 / Accepted: 9 January 2014 / Published: 20 January 2014
Cited by 7 | PDF Full-text (2087 KB) | HTML Full-text | XML Full-text
Abstract
High-protein diets have been shown to prevent the development of diet-induced obesity and can improve associated metabolic disorders in mice. Dietary leucine supplementation can partially mimic this effect. However, the molecular mechanisms triggering these preventive effects remain to be satisfactorily explained. Here we
[...] Read more.
High-protein diets have been shown to prevent the development of diet-induced obesity and can improve associated metabolic disorders in mice. Dietary leucine supplementation can partially mimic this effect. However, the molecular mechanisms triggering these preventive effects remain to be satisfactorily explained. Here we review studies showing a connection between high protein or total amino nitrogen intake and obligatory water intake. High amino nitrogen intake may possibly lower lipid storage, and prevent insulin resistance. Suggestions are made for further systematical studies to explore the relationship between water consumption, satiety, and energy expenditure. Moreover, these examinations should better distinguish between leucine-specific and unspecific effects. Research in this field can provide important information to justify dietary recommendations and strategies in promoting long-term weight loss and may help to reduce health problems associated with the comorbidities of obesity. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Open AccessReview Biological Significance of Calbindin-D9k within Duodenal Epithelium
Int. J. Mol. Sci. 2013, 14(12), 23330-23340; doi:10.3390/ijms141223330
Received: 28 October 2013 / Revised: 22 November 2013 / Accepted: 22 November 2013 / Published: 26 November 2013
PDF Full-text (458 KB) | HTML Full-text | XML Full-text
Abstract
Calbindin-D9k (CaBP-9k) binds calcium with high affinity and regulates the distribution of free calcium in the cytoplasm. The expression of CaBP-9k is detected primarily in intestine that is vitamin D target tissue, and accumulates in the enterocytes of the duodenal villi. These
[...] Read more.
Calbindin-D9k (CaBP-9k) binds calcium with high affinity and regulates the distribution of free calcium in the cytoplasm. The expression of CaBP-9k is detected primarily in intestine that is vitamin D target tissue, and accumulates in the enterocytes of the duodenal villi. These enterocytes are the clearest example of vitamin D responsive cells, and the presence of CaBP-9k within them accentuates calcium absorption mediated by active transcellular calcium transport. It has been well established that the expression of CaBP-9k is mediated with vitamin D response element on its promoter and it regulates the amount of intracellular calcium in order to prevent cell death from reaching the toxicity of free calcium. There is now little doubt that glucocorticoid also decreases CaBP-9k expression in duodenal epithelial cells. In addition, it was reported that the level of CaBP-9k gene in enterocytes is increased in pregnancy when the plasma estradiol concentration is generally associated with a concomitant increase. Although calcium homeostasis was not disturbed in mice lacking the CaBP-9k gene, we found that CaBP-9k has a buffering role of free calcium in the cytosolic environment beyond that of calcium transfer. To expand our knowledge of the biological functions of CaBP-9k, our research has focused on defining the biological significance of intracellular CaBP-9k. Our findings suggest that the CaBP-9k gene is involved in compensatory induction of other calcium transporter genes in duodenal epithelial cells. This article summarizes the findings from recent studies on the expression and the functions of CaBP-9k in the small intestine. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)

Other

Jump to: Research, Review

Open AccessConcept Paper Docosahexaenoic Acid Supplementation during Pregnancy: A Potential Tool to Prevent Membrane Rupture and Preterm Labor
Int. J. Mol. Sci. 2014, 15(5), 8024-8036; doi:10.3390/ijms15058024
Received: 17 March 2014 / Revised: 24 April 2014 / Accepted: 29 April 2014 / Published: 7 May 2014
Cited by 3 | PDF Full-text (1088 KB) | HTML Full-text | XML Full-text
Abstract
Polyunsaturated fatty acids (PUFAs) are required to maintain the fluidity, permeability and integrity of cell membranes. Maternal dietary supplementation with ω-3 PUFAs during pregnancy has beneficial effects, including increased gestational length and reduced risk of pregnancy complications. Significant amounts of ω-3 docosahexaenoic acid
[...] Read more.
Polyunsaturated fatty acids (PUFAs) are required to maintain the fluidity, permeability and integrity of cell membranes. Maternal dietary supplementation with ω-3 PUFAs during pregnancy has beneficial effects, including increased gestational length and reduced risk of pregnancy complications. Significant amounts of ω-3 docosahexaenoic acid (DHA) are transferred from maternal to fetal blood, hence ensuring high levels of DHA in the placenta and fetal bloodstream and tissues. Fetal DHA demand increases exponentially with gestational age, especially in the third trimester, due to fetal development. According to the World Health Organization (WHO) and the Food and Agriculture Organization of the United Nations (FAO), a daily intake of DHA is recommended during pregnancy. Omega-3 PUFAs are involved in several anti-inflammatory, pro-resolving and anti-oxidative pathways. Several placental disorders, such as intrauterine growth restriction, premature rupture of membranes (PROM) and preterm-PROM (pPROM), are associated with placental inflammation and oxidative stress. This pilot study reports on a preliminary evaluation of the significance of the daily DHA administration on PROM and pPROM events in healthy pregnant women. Further extensive clinical trials will be necessary to fully elucidate the correlation between DHA administration during pregnancy and PROM/pPROM occurrence, which is related in turn to gestational duration and overall fetal health. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)
Figures

Open AccessComment Calcium and Vitamin D in the Regulation of Energy Balance: Where Do We Stand?
Int. J. Mol. Sci. 2014, 15(3), 4938-4945; doi:10.3390/ijms15034938
Received: 19 February 2014 / Revised: 11 March 2014 / Accepted: 13 March 2014 / Published: 20 March 2014
Cited by 13 | PDF Full-text (248 KB) | HTML Full-text | XML Full-text
Abstract
There is a pandemic of obesity and associated chronic diseases. Dietary calcium and vitamin D have many extra-skeletal roles in human health. In this review we have summarized the current understanding of their influence on human energy balance by examining the epidemiological, clinical,
[...] Read more.
There is a pandemic of obesity and associated chronic diseases. Dietary calcium and vitamin D have many extra-skeletal roles in human health. In this review we have summarized the current understanding of their influence on human energy balance by examining the epidemiological, clinical, animal, cellular and molecular evidence. We opine that while calcium and vitamin D are functional nutrients in the battle against obesity, there is a need for prospective human trials to tilt the balance of evidence in favour of these nutrients. Full article
(This article belongs to the Special Issue Nutritional Control of Metabolism)

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