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The Role of Nutrition in Cardiometabolic Health: Experimental, Clinical, and Community-Based Evidence

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutritional Epidemiology".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 59094

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Special Issue Editors


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Guest Editor
Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA
Interests: cardiovascular disease; obesity; diabetes; metabolic disease; vascular biology; exercise physiology; molecular biology; pathology; nutrition; epigenetics; translational research; dietary interventions; biomarkers; chemoprevention; cancer biology; racial disparity; clinical trials
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Guest Editor
Department of Physical Therapy, College of Applied Health Sciences, University of Illinois at Chicago, Chicago, IL 60612, USA
Interests: vascular biology; clinical trials; exercise physiology; physical therapy; obesity; racial disparity; cardiovascular research; dietary interventions; translational research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The purpose of this Special Issue “The Role of Nutrition in Cardiometabolic Health: Experimental, Clinical, and Community-Based Evidence” is to publish a focused, coherent, impactful, and well-cited volume on how nutrition influences diverse cardiometabolic risk factors. Cardiometabolic diseases, such as coronary heart disease, stroke, type 2 diabetes mellitus, and obesity, is the leading cause of death worldwide. In recent years, dietary habits have shifted all over the globe. At the same time, a constantly growing body of evidence demonstrates the role of caloric intake and dietary composition as determinants of cardiometabolic health. Suboptimal diet predisposes to a myriad of cardiometabolic risk factors such as impaired glucose metabolism, insulin resistance, dyslipidaemias, and high blood pressure. The goal of this Special Issue is to provide rigorous evidence from novel experimental and observational studies that support the association between dietary factors and cardiometabolic risk and evaluate the diverse diet-related risk pathways. Both original and review articles are acceptable. Articles of a basic science nature, animal studies, clinical/translational studies, epidemiological studies, meta-analyses, and behavioral studies are acceptable. Potential topics include, but are not limited to:

  • effects of dietary patterns, nutrients (macro and micro), or supplements on vascular biology and/or physiology and endothelial health, inflammation and oxidative stress, glucose and insulin homeostasis, lipid and energy metabolism, blood pressure and cardiac function, metabolic expenditure and pathways of weight regulation, visceral adiposity and adipocyte metabolism, the gut microbiome, liver function and non-alcoholic steatohepatitis, coronary artery disease, atherosclerosis, and stroke;
  • cellular, molecular, and epigenetic pathways that are modified by dietary factors and contribute to cardiometabolic health;
  • genetic, environmental, and socioeconomic factors that affect dietary behavior and cardiometabolic outcomes;
  • nutritional considerations for optimal cardiometabolic health;
  • obesity and eating disorders in adults and children and how they modulate cardiometabolic risk;
  • nutrition, physical activity, and bariatric surgery in relation to cardiometabolic health; and
  • effects of plant-derived phytochemicals and bioactive compounds in cardiometabolic health.

Dr. Abeer M. Mahmoud
Prof. Shane Phillips
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly 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 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diet
  • risk factor
  • nutrition
  • supplements
  • caloric restriction
  • cardiometabolic
  • obesity
  • diabetes
  • glucose metabolism
  • insulin resistance
  • lipid profile
  • vascular biology
  • endothelial function
  • cardiovascular
  • nutrigenomics
  • epigenetics
  • weight loss
  • metabolism
  • coronary artery disease
  • stroke
  • hypertension
  • atherosclerosis
  • inflammation
  • oxidative stress
  • phytochemicals
  • bariatric surgery
  • microbiome

Published Papers (11 papers)

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Research

Jump to: Review

15 pages, 1158 KiB  
Article
The Cardiotonic Steroid Marinobufagenin Is a Predictor of Increased Left Ventricular Mass in Obesity: The African-PREDICT Study
by Michél Strauss-Kruger, Ruan Kruger, Wayne Smith, Lebo F. Gafane-Matemane, Gontse Mokwatsi, Wen Wei, Olga V. Fedorova and Aletta E. Schutte
Nutrients 2020, 12(10), 3185; https://doi.org/10.3390/nu12103185 - 18 Oct 2020
Cited by 7 | Viewed by 2524
Abstract
The endogenous Na+/K+-ATPase inhibitor, marinobufagenin (MBG), strongly associates with salt intake and a greater left ventricular mass index (LVMi) in humans and was shown to promote cardiac fibrosis and hypertrophy in animals. The adverse effects of MBG on cardiac [...] Read more.
The endogenous Na+/K+-ATPase inhibitor, marinobufagenin (MBG), strongly associates with salt intake and a greater left ventricular mass index (LVMi) in humans and was shown to promote cardiac fibrosis and hypertrophy in animals. The adverse effects of MBG on cardiac remodeling may be exacerbated with obesity, due to an increased sensitivity of Na+/K+-ATPase to MBG. This study determined whether MBG is related to the change in LVMi over time in adults with a body mass index (BMI) ≥30 kg/m2 (obese) and <30 kg/m2 (non-obese). The study followed 275 healthy participants (aged 20–30 years) from the African-Prospective study on the Early Detection and Identification of Cardiovascular disease and Hypertension (African-PREDICT) study over 4.5 years. At baseline, we measured 24 h urine MBG excretion. MBG levels were positively associated with salt intake. LVMi was determined by two-dimensional echocardiography at baseline and after >4.5 years. With multivariate adjusted analyses in obese adults (N = 56), we found a positive association of follow-up LVMi (Adjusted (Adj.) R2 = 0.35; Std. β = 0.311; p = 0.007) and percentage change in LVMi (Adj. R2 = 0.40; Std. β = 0.336; p = 0.003) with baseline MBG excretion. No association of LVMi (Adj. R2 = 0.37; p = 0.85) or percentage change in LVMi (Adj. R2 = 0.19; p = 0.68) with MBG excretion was evident in normal weight adults (N = 123). These findings suggest that obese adults may be more sensitive to the adverse cardiac effects of MBG and provide new insight into the potential role of dietary salt, by way of MBG, in the pathogenesis of cardiac remodeling in obese individuals. Full article
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15 pages, 3757 KiB  
Article
No Effect of Diet-Induced Mild Hyperhomocysteinemia on Vascular Methylating Capacity, Atherosclerosis Progression, and Specific Histone Methylation
by Courtney A. Whalen, Floyd J. Mattie, Cristina Florindo, Bertrand van Zelst, Neil K. Huang, Isabel Tavares de Almeida, Sandra G. Heil, Thomas Neuberger, A. Catharine Ross and Rita Castro
Nutrients 2020, 12(8), 2182; https://doi.org/10.3390/nu12082182 - 23 Jul 2020
Cited by 8 | Viewed by 2878
Abstract
Hyperhomocysteinemia (HHcy) is a risk factor for atherosclerosis through mechanisms which are still incompletely defined. One possible mechanism involves the hypomethylation of the nuclear histone proteins to favor the progression of atherosclerosis. In previous cell studies, hypomethylating stress decreased a specific epigenetic tag [...] Read more.
Hyperhomocysteinemia (HHcy) is a risk factor for atherosclerosis through mechanisms which are still incompletely defined. One possible mechanism involves the hypomethylation of the nuclear histone proteins to favor the progression of atherosclerosis. In previous cell studies, hypomethylating stress decreased a specific epigenetic tag (the trimethylation of lysine 27 on histone H3, H3K27me3) to promote endothelial dysfunction and activation, i.e., an atherogenic phenotype. Here, we conducted a pilot study to investigate the impact of mild HHcy on vascular methylating index, atherosclerosis progression and H3K27me3 aortic content in apolipoprotein E-deficient (ApoE −/−) mice. In two different sets of experiments, male mice were fed high-fat, low in methyl donors (HFLM), or control (HF) diets for 16 (Study A) or 12 (Study B) weeks. At multiple time points, plasma was collected for (1) quantification of total homocysteine (tHcy) by high-performance liquid chromatography; or (2) the methylation index of S-adenosylmethionine to S-adenosylhomocysteine (SAM:SAH ratio) by liquid chromatography tandem-mass spectrometry; or (3) a panel of inflammatory cytokines previously implicated in atherosclerosis by a multiplex assay. At the end point, aortas were collected and used to assess (1) the methylating index (SAM:SAH ratio); (2) the volume of aortic atherosclerotic plaque assessed by high field magnetic resonance imaging; and (3) the vascular content of H3K27me3 by immunohistochemistry. The results showed that, in both studies, HFLM-fed mice, but not those mice fed control diets, accumulated mildly elevated tHcy plasmatic concentrations. However, the pattern of changes in the inflammatory cytokines did not support a major difference in systemic inflammation between these groups. Accordingly, in both studies, no significant differences were detected for the aortic methylating index, plaque burden, and H3K27me3 vascular content between HF and HFLM-fed mice. Surprisingly however, a decreased plasma SAM: SAH was also observed, suggesting that the plasma compartment does not always reflect the vascular concentrations of these two metabolites, at least in this model. Mild HHcy in vivo was not be sufficient to induce vascular hypomethylating stress or the progression of atherosclerosis, suggesting that only higher accumulations of plasma tHcy will exhibit vascular toxicity and promote specific epigenetic dysregulation. Full article
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12 pages, 2570 KiB  
Article
Compound 18 Improves Glucose Tolerance in a Hepatocyte TGR5-dependent Manner in Mice
by Marlena M. Holter, Margot K. Chirikjian, Daniel A. Briere, Adriano Maida, Kyle W. Sloop, Kristina Schoonjans and Bethany P. Cummings
Nutrients 2020, 12(7), 2124; https://doi.org/10.3390/nu12072124 - 17 Jul 2020
Cited by 15 | Viewed by 3370
Abstract
The bile acid receptor, TGR5, is a key regulator of glucose homeostasis, but the mechanisms by which TGR5 signaling improves glucose regulation are incompletely defined. In particular, TGR5 has an increasingly appreciated role in liver physiology and pathobiology; however, whether TGR5 signaling within [...] Read more.
The bile acid receptor, TGR5, is a key regulator of glucose homeostasis, but the mechanisms by which TGR5 signaling improves glucose regulation are incompletely defined. In particular, TGR5 has an increasingly appreciated role in liver physiology and pathobiology; however, whether TGR5 signaling within the liver contributes to its glucoregulatory effects is unknown. Therefore, we investigated the role of hepatocyte TGR5 signaling on glucose regulation using a hepatocyte-specific TGR5 knockout mouse model. Hepatocyte-specific Tgr5Hep+/+ and Tgr5Hep−/− mice were fed a high fat diet (HFD) for 7 weeks and then orally gavaged with three doses of a highly potent, TGR5-specific agonist, Compound 18 (10 mg/kg), or vehicle, over 72 h and underwent an oral glucose tolerance test (OGTT) after the last dose. Herein, we report that TGR5 mRNA and protein is present in mouse hepatocytes. Cumulative food intake, body weight, and adiposity do not differ between Tgr5Hep+/+ and Tgr5Hep−/− mice with or without treatment with Compound 18. However, administration of Compound 18 improves glucose tolerance in Tgr5HEP+/+ mice, but not in Tgr5Hep−/− mice. Further, this effect occurred independent of body weight and GLP-1 secretion. Together, these data demonstrate that TGR5 is expressed in hepatocytes, where it functions as a key regulator of whole-body glucose homeostasis. Full article
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21 pages, 4104 KiB  
Article
Hyperhomocysteinemia and Low Folate and Vitamin B12 Are Associated with Vascular Dysfunction and Impaired Nitric Oxide Sensitivity in Morbidly Obese Patients
by Mohamed Haloul, Smita Jagdish Vinjamuri, Dina Naquiallah, Mohammed Imaduddin Mirza, Maryam Qureshi, Chandra Hassan, Mario Masrur, Francesco M. Bianco, Patrice Frederick, Giulianotti P. Cristoforo, Antonio Gangemi, Mohamed M. Ali, Shane A. Phillips and Abeer M. Mahmoud
Nutrients 2020, 12(7), 2014; https://doi.org/10.3390/nu12072014 - 7 Jul 2020
Cited by 25 | Viewed by 5124
Abstract
There is a high prevalence of hyperhomocysteinemia that has been linked to high cardiovascular risk in obese individuals and could be attributed to poor nutritional status of folate and vitamin B12. We sought to examine the association between blood homocysteine (Hcy) folate, and [...] Read more.
There is a high prevalence of hyperhomocysteinemia that has been linked to high cardiovascular risk in obese individuals and could be attributed to poor nutritional status of folate and vitamin B12. We sought to examine the association between blood homocysteine (Hcy) folate, and vitamin B12 levels and vascular dysfunction in morbidly obese adults using novel ex vivo flow-induced dilation (FID) measurements of isolated adipose tissue arterioles. Brachial artery flow-mediated dilation (FMD) was also measured. Subcutaneous and visceral adipose tissue biopsies were obtained from morbidly obese individuals and non-obese controls. Resistance arterioles were isolated in which FID, acetylcholine-induced dilation (AChID), and nitric oxide (NO) production were measured in the absence or presence of the NO synthase inhibitor, L-NAME, Hcy, or the superoxide dismutase mimetic, TEMPOL. Our results demonstrated that plasma Hcy concentrations were significantly higher, while folate, vitamin B12, and NO were significantly lower in obese subjects compared to controls. Hcy concentrations correlated positively with BMI, fat %, and insulin levels but not with folate or vitamin B12. Brachial and arteriolar vasodilation were lower in obese subjects, positively correlated with folate and vitamin B12, and inversely correlated with Hcy. Arteriolar NO measurements and sensitivity to L-NAME were lower in obese subjects compared to controls. Finally, Hcy incubation reduced arteriolar FID and NO sensitivity, an effect that was abolished by TEMPOL. In conclusion, these data suggest that high concentrations of plasma Hcy and low concentrations of folate and vitamin B12 could be independent predictors of vascular dysfunction in morbidly obese individuals. Full article
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15 pages, 921 KiB  
Article
The Effect of Low-Carbohydrate Diet on Macrovascular and Microvascular Endothelial Function Is Not Affected by the Provision of Caloric Restriction in Women with Obesity: A Randomized Study
by Chueh-Lung Hwang, Christine Ranieri, Mary R. Szczurek, Assem M. Ellythy, Ahmed Elokda, Abeer M. Mahmoud and Shane A. Phillips
Nutrients 2020, 12(6), 1649; https://doi.org/10.3390/nu12061649 - 2 Jun 2020
Cited by 9 | Viewed by 7507
Abstract
Obesity impairs both macro- and microvascular endothelial function due to decreased bioavailability of nitric oxide. Current evidence on the effect of low-carbohydrate (LC) diet on endothelial function is conflicting and confounded by the provision of caloric restriction (CR). We tested the hypothesis that [...] Read more.
Obesity impairs both macro- and microvascular endothelial function due to decreased bioavailability of nitric oxide. Current evidence on the effect of low-carbohydrate (LC) diet on endothelial function is conflicting and confounded by the provision of caloric restriction (CR). We tested the hypothesis that LC without CR diet, but not LC with CR diet, would improve macro- and microvascular endothelial function in women with obesity. Twenty-one healthy women with obesity (age: 33 ± 2 years, body mass index: 33.0 ± 0.6 kg/m2; mean ± SEM) were randomly assigned to receive either a LC diet (~10% carbohydrate calories) with CR (n = 12; 500 calorie/day deficit) or a LC diet without CR (n = 9) and completed the 6-week diet intervention. After the intervention, macrovascular endothelial function, measured as brachial artery flow-mediated dilation did not change (7.3 ± 0.9% to 8.0 ± 1.1%, p = 0.7). On the other hand, following the LC diet intervention, regardless of CR, blocking nitric oxide production decreased microvascular endothelial function, measured by arteriolar flow-induced dilation (p ≤ 0.02 for both diets) and the magnitude was more than baseline (p ≤ 0.04). These data suggest improved NO contributions following the intervention. In conclusion, a 6-week LC diet, regardless of CR, may improve microvascular, but not macrovascular endothelial function, via increasing bioavailability of nitric oxide in women with obesity. Full article
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18 pages, 748 KiB  
Article
Effects of Whey Protein Supplementation on Aortic Stiffness, Cerebral Blood Flow, and Cognitive Function in Community-Dwelling Older Adults: Findings from the ANCHORS A-WHEY Clinical Trial
by Wesley K. Lefferts, Jacqueline A. Augustine, Nicole L. Spartano, William E. Hughes, Matthew C. Babcock, Brigid K. Heenan and Kevin S. Heffernan
Nutrients 2020, 12(4), 1054; https://doi.org/10.3390/nu12041054 - 10 Apr 2020
Cited by 8 | Viewed by 5214
Abstract
ANCHORS A-WHEY was a 12-week randomized controlled trial (RCT) designed to examine the effect of whey protein on large artery stiffness, cerebrovascular responses to cognitive activity and cognitive function in older adults. Methods: 99 older adults (mean ± SD; age 67 ± 6 [...] Read more.
ANCHORS A-WHEY was a 12-week randomized controlled trial (RCT) designed to examine the effect of whey protein on large artery stiffness, cerebrovascular responses to cognitive activity and cognitive function in older adults. Methods: 99 older adults (mean ± SD; age 67 ± 6 years, BMI 27.2 ± 4.7kg/m2, 45% female) were randomly assigned to 50g/daily of whey protein isolate (WPI) or an iso-caloric carbohydrate (CHO) control for 12 weeks (NCT01956994). Aortic stiffness was determined as carotid-femoral pulse wave velocity (cfPWV). Aortic hemodynamic load was assessed as the product of aortic systolic blood pressure and heart rate (Ao SBP × HR). Cerebrovascular response to cognitive activity was assessed as change in middle-cerebral artery (MCA) blood velocity pulsatility index (PI) during a cognitive perturbation (Stroop task). Cognitive function was assessed using a computerized neurocognitive battery. Results: cfPWV increased slightly in CHO and significantly decreased in WPI (p < 0.05). Ao SBP × HR was unaltered in CHO but decreased significantly in WPI (p < 0.05). Although emotion recognition selectively improved with WPI (p < 0.05), WPI had no effect on other domains of cognitive function or MCA PI response to cognitive activity (p > 0.05 for all). Conclusions: Compared to CHO, WPI supplementation results in favorable reductions in aortic stiffness and aortic hemodynamic load with limited effects on cognitive function and cerebrovascular function in community-dwelling older adults. Full article
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15 pages, 3839 KiB  
Article
Temporal Measures in Cardiac Structure and Function During the Development of Obesity Induced by Different Types of Western Diet in a Rat Model
by Danielle Fernandes Vileigas, Cecília Lume de Carvalho Marciano, Gustavo Augusto Ferreira Mota, Sérgio Luiz Borges de Souza, Paula Grippa Sant’Ana, Katashi Okoshi, Carlos Roberto Padovani and Antonio Carlos Cicogna
Nutrients 2020, 12(1), 68; https://doi.org/10.3390/nu12010068 - 26 Dec 2019
Cited by 8 | Viewed by 3538
Abstract
Obesity is recognized worldwide as a complex metabolic disorder that has reached epidemic proportions and is often associated with a high incidence of cardiovascular diseases. To study this pathology and evaluate cardiac function, several models of diet-induced obesity (DIO) have been developed. The [...] Read more.
Obesity is recognized worldwide as a complex metabolic disorder that has reached epidemic proportions and is often associated with a high incidence of cardiovascular diseases. To study this pathology and evaluate cardiac function, several models of diet-induced obesity (DIO) have been developed. The Western diet (WD) is one of the most widely used models; however, variations in diet composition and time period of the experimental protocol make comparisons challenging. Thus, this study aimed to evaluate the effects of two different types of Western diet on cardiac remodeling in obese rats with sequential analyses during a long-term follow-up. Male Wistar rats were distributed into three groups fed with control diet (CD), Western diet fat (WDF), and Western diet sugar (WDS) for 41 weeks. The animal nutritional profile and cardiac histology were assessed at the 41st week. Cardiac structure and function were evaluated by echocardiogram at four different moments: 17, 25, 33, and 41 weeks. A noninvasive method was performed to assess systolic blood pressure at the 33rd and 41st week. The animals fed with WD (WDF and WDS) developed pronounced obesity with an average increase of 86.5% in adiposity index at the end of the experiment. WDF and WDS groups also presented hypertension. The echocardiographic data showed no structural differences among the three groups, but WDF animals presented decreased endocardial fractional shortening and ejection fraction at the 33rd and 41st week, suggesting altered systolic function. Moreover, WDF and WFS animals did not present hypertrophy and interstitial collagen accumulation in the left ventricle. In conclusion, both WD were effective in triggering severe obesity in rats; however, only the WDF induced mild cardiac dysfunction after long-term diet exposure. Further studies are needed to search for an appropriate DIO model with relevant cardiac remodeling. Full article
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19 pages, 4008 KiB  
Article
Vitamin D Improves Nitric Oxide-Dependent Vasodilation in Adipose Tissue Arterioles from Bariatric Surgery Patients
by Abeer M. Mahmoud, Mary Szczurek, Chandra Hassan, Mario Masrur, Antonio Gangemi and Shane A. Phillips
Nutrients 2019, 11(10), 2521; https://doi.org/10.3390/nu11102521 - 18 Oct 2019
Cited by 15 | Viewed by 4419
Abstract
There is a high prevalence of vitamin-D deficiency in obese individuals that could be attributed to vitamin-D sequestration in the adipose tissue. Associations between vitamin-D deficiency and unfavorable cardiometabolic outcomes were reported. However, the pathophysiological mechanisms behind these associations are yet to be [...] Read more.
There is a high prevalence of vitamin-D deficiency in obese individuals that could be attributed to vitamin-D sequestration in the adipose tissue. Associations between vitamin-D deficiency and unfavorable cardiometabolic outcomes were reported. However, the pathophysiological mechanisms behind these associations are yet to be established. In our previous studies, we demonstrated microvascular dysfunction in obese adults that was associated with reduced nitric oxide (NO) production. Herein, we examined the role of vitamin D in mitigating microvascular function in morbidly obese adults before and after weight loss surgery. We obtained subcutaneous (SAT) and visceral adipose tissue (VAT) biopsies from bariatric patients at the time of surgery (n = 15) and gluteal SAT samples three months post-surgery (n = 8). Flow-induced dilation (FID) and acetylcholine-induced dilation (AChID) and NO production were measured in the AT-isolated arterioles ± NO synthase inhibitor N(ω)-nitro-L-arginine methyl ester (L-NAME), hydrogen peroxide (H2O2) inhibitor, polyethylene glycol-modified catalase (PEG-CAT), or 1,25-dihydroxyvitamin D. Vitamin D improved FID, AChID, and NO production in AT-isolated arterioles at time of surgery; these effects were abolished by L-NAME but not by PEG-CAT. Vitamin-D-mediated improvements were of a higher magnitude in VAT compared to SAT arterioles. After surgery, significant improvements in FID, AChID, NO production, and NO sensitivity were observed. Vitamin-D-induced changes were of a lower magnitude compared to those from the time of surgery. In conclusion, vitamin D improved NO-dependent arteriolar vasodilation in obese adults; this effect was more significant before surgery-induced weight loss. Full article
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Review

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12 pages, 275 KiB  
Review
Micronutrient Deficiencies in Laparoscopic Sleeve Gastrectomy
by Omar Jamil, Raquel Gonzalez-Heredia, Pablo Quadri, Chandra Hassan, Mario Masrur, Reed Berger, Karen Bernstein and Lisa Sanchez-Johnsen
Nutrients 2020, 12(9), 2896; https://doi.org/10.3390/nu12092896 - 22 Sep 2020
Cited by 5 | Viewed by 3608
Abstract
The purpose of this study was to conduct a literature review to examine micronutrient deficiencies in laparoscopic sleeve gastrectomy. We conducted a literature review using PubMed and Cochrane databases to examine micronutrient deficiencies in SG patients in order to identify trends and find [...] Read more.
The purpose of this study was to conduct a literature review to examine micronutrient deficiencies in laparoscopic sleeve gastrectomy. We conducted a literature review using PubMed and Cochrane databases to examine micronutrient deficiencies in SG patients in order to identify trends and find consistency in recommendations. Seventeen articles were identified that met the defined criteria. Iron, vitamin B12 and vitamin D were the primary micronutrients evaluated. Results demonstrate the need for consistent iron and B12 supplementation, in addition to a multivitamin, while vitamin D supplementation may not be necessary. Additional prospective studies to establish a clearer picture of micronutrient deficiencies post-SG are needed. Full article
15 pages, 1884 KiB  
Review
TGR5 Signaling in Hepatic Metabolic Health
by Marlena M. Holter, Margot K. Chirikjian, Viraj N. Govani and Bethany P. Cummings
Nutrients 2020, 12(9), 2598; https://doi.org/10.3390/nu12092598 - 26 Aug 2020
Cited by 40 | Viewed by 7218
Abstract
TGR5 is a G protein-coupled bile acid receptor that is increasingly recognized as a key regulator of glucose homeostasis. While the role of TGR5 signaling in immune cells, adipocytes and enteroendocrine L cells in metabolic regulation has been well described and extensively reviewed, [...] Read more.
TGR5 is a G protein-coupled bile acid receptor that is increasingly recognized as a key regulator of glucose homeostasis. While the role of TGR5 signaling in immune cells, adipocytes and enteroendocrine L cells in metabolic regulation has been well described and extensively reviewed, the impact of TGR5-mediated effects on hepatic physiology and pathophysiology in metabolic regulation has received less attention. Recent studies suggest that TGR5 signaling contributes to improvements in hepatic insulin signaling and decreased hepatic inflammation, as well as metabolically beneficial improvements in bile acid profile. Additionally, TGR5 signaling has been associated with reduced hepatic steatosis and liver fibrosis, and improved liver function. Despite the beneficial effects of TGR5 signaling on metabolic health, TGR5-mediated gallstone formation and gallbladder filling complicate therapeutic targeting of TGR5 signaling. To this end, there is a growing need to identify cell type-specific effects of hepatic TGR5 signaling to begin to identify and target the downstream effectors of TGR5 signaling. Herein, we describe and integrate recent advances in our understanding of the impact of TGR5 signaling on liver physiology and how its effects on the liver integrate more broadly with whole body glucose regulation. Full article
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18 pages, 1777 KiB  
Review
Dietary Factors and Risks of Cardiovascular Diseases: An Umbrella Review
by Kridsada Chareonrungrueangchai, Keerati Wongkawinwoot, Thunyarat Anothaisintawee and Sirimon Reutrakul
Nutrients 2020, 12(4), 1088; https://doi.org/10.3390/nu12041088 - 15 Apr 2020
Cited by 71 | Viewed by 12530
Abstract
Unhealthy diet is a significant risk factor for cardiovascular diseases (CVD). Therefore, this umbrella review aims to comprehensively review the effects of dietary factors, including dietary patterns, food groups, and nutrients on CVD risks. Medline and Scopus databases were searched through March 2020. [...] Read more.
Unhealthy diet is a significant risk factor for cardiovascular diseases (CVD). Therefore, this umbrella review aims to comprehensively review the effects of dietary factors, including dietary patterns, food groups, and nutrients on CVD risks. Medline and Scopus databases were searched through March 2020. Systematic reviews with meta-analyses (SRMA) of randomized controlled trials (RCTs) or observational studies measuring the effects of dietary factors on CVD risks were eligible. Fifty-four SRMAs, including 35 SRMAs of observational studies, 10 SRMAs of RCTs, and 9 SRMAs of combined RCT and observational studies, were included for review. Findings from the SRMAs of RCTs suggest the significant benefit of Mediterranean and high-quality diets for lowering CVD risk, with pooled risk ratios (RRs) ranging from 0.55 (95%CI: 0.39–0.76) to 0.64 (95%CI: 0.53–0.79) and 0.70 (95%CI: 0.57–0.87), respectively. For food nutrients, two SRMAs of RCTs found that high intake of n-3 polyunsaturated fatty acid (PUFA) significantly reduced CVD risks, with pooled RRs ranging from 0.89 (95%CI: 0.82, 0.98) to 0.90 (95%CI: 0.85–0.96), while evidence of efficacy of n-6 PUFA and combined n-3 and n-6 PUFA were inconsistent. Moreover, results from the SRMAs of RCTs did not find a significant benefit of a low-salt diet and low total fat intake for CVD prevention. For food groups, results from the SRMAs of cohort studies suggest that high intakes of legumes, nuts, and chocolate, as well as a vegetarian diet significantly reduced the risk of coronary heart disease, with pooled RRs of 0.90 (95%CI: 0.84–0.97), 0.68 (95%CI: 0.59–0.78), 0.90 (95%CI: 0.82–0.97), and 0.71 (95%CI: 0.57–0.87), respectively. Healthy dietary patterns had a significant benefit for CVD prevention. With the substitutional and synergistic interactions between different food groups and nutrients, dietary recommendations for CVD prevention should be focused more on healthy dietary patterns than single food groups or nutrients. Full article
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