Serum Level of Uromodulin as an Early Predictor Marker of Kidney Disorders

BACKGROUND: Metabolic diseases are known to be risk factors of kidney injury. The glycoprotein Uromodulin Tamm-Horsfall protein is a biochemical marker specifically synthesized and secreted by kidney tubular epithelial cells. AIM: The study aimed to use novel biochemical parameters to predict early changes in renal functions and to use natural food supplements to help in the prevention and management of such conditions. METHODS: Crossover studies comparing two interventions trials. Subjects: Seventy obese females were included in this study. They were divided in two groups, first group (34 women) with mean age 45.82 ± 1.51 and mean body mass index (BMI) 35.65 ± 0.68 kg/m2, and second group (36 women) with mean age 49.80 ± 2.27, and mean BMI 37.67 ± 1.59. Intervention: All participants have followed a low caloric balanced regimen (1000–1200 Kcal/day) of the each groups consumed a different specific nutritional supplement composed mainly of whole grains and herbs. All patients were monitored clinically, anthropometrically, dietary 24 h recall and biochemically. RESULTS: After intervention all the recorded anthropometric parameters showed significant decreases at p ≤ 0.05–0.01. The serum uromodulin (sUMOD) increased significantly after intervention in both groups the increments were 15.56 and 9.37%. Numerically creatinine and urea decreased, while creatinine clearance increased. CONCLUSION: Data revealed the importance of using dietary therapy composed of hypocaloric diet with supplements made from whole grains and special herbs in management of obesity and its metabolic disorders. sUMOD proved to be an accurate biochemical marker that showed the kidneys’ response to the management in comparison to using usual diagnostic markers.

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The Effects of Coenzyme Q10 Supplementation on Lipid Profiles Among Patients with Metabolic Diseases: A Systematic Review and Meta-analysis of Randomized Controlled Trials

Current Pharmaceutical Design ◽

10.2174/1381612824666180406104516 ◽

2018 ◽

Vol 24 (23) ◽

pp. 2729-2742 ◽

Cited By ~ 6

Author(s):

Nasrin Sharifi ◽

Reza Tabrizi ◽

Mahmood Moosazadeh ◽

Naghmeh Mirhosseini ◽

Kamran B. Lankarani ◽

...

Keyword(s):

Systematic Review ◽

Lipid Profile ◽

Coenzyme Q10 ◽

Metabolic Disorders ◽

Metabolic Diseases ◽

Meta Analysis ◽

Lipid Profiles ◽

Controlled Trials ◽

Serum Triglycerides ◽

Coq10 Supplementation

Background and objective: Oxidative stress and inflammation are key parameters in developing metabolic disorders. Hence, antioxidant intake might be an appropriate approach. Several studies have evaluated the effect of coenzyme Q10 (CoQ10) supplementation on lipid profile among patients with metabolic diseases, though findings are controversial. The aim of this systematic review and meta-analysis was to determine the effects of CoQ10 supplementation on lipid profile in patients with metabolic disorders. Methods: We searched PubMed, EMBASE, Web of Science and Cochrane Library databases until July 2017. Prospective clinical trials were selected assessing the effect of CoQ10 supplementation on different biomarkers. Two reviewers independently assessed the eligibility of studies, extracted data, and evaluated the risk of bias of included studies. A fixed- or random-effects model was used to pool the data, which expressed as a standardized mean difference with 95% confidence interval. Heterogeneity was measured using a Q-test and with I2 statistics. Results: A total of twenty-one controlled trials (514 patients and 525 controls) were included. The meta-analysis indicated a significant reduction in serum triglycerides levels (SMD -0.28; 95% CI, -0.56, -0.005). CoQ10 supplementation also decreased total-cholesterol (SMD -0.07; 95% CI, -0.45, 0.31), increased LDL- (SMD 0.04; 95% CI, -0.27, 0.36), and HDL-cholesterol levels (SMD 0.10; 95% CI, -0.32, 0.51), not statistically significant. Conclusion: CoQ10 supplementation may significantly reduce serum triglycerides levels, and help to improve lipid profiles in patients with metabolic disorders. Additional prospective studies are recommended using higher supplementation doses and longer intervention period.

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INHERITED METABOLIC DISORDERS AND HEART DISEASES

10.5644/pi2019.181.02 ◽

2019 ◽

Author(s):

Vjekoslav Krželj ◽

Ivana Čulo Čagalj

Keyword(s):

Metabolic Disorders ◽

Metabolic Diseases ◽

Technological Development ◽

Heart Diseases ◽

Glycogen Storage ◽

Acid Oxidation ◽

Lysosomal Storage ◽

Glycogen Storage Diseases ◽

Coronary Diseases ◽

Inherited Metabolic Disorders

Inherited metabolic disorders can cause heart diseases, cardiomyopathy in particular, as well as cardiac arrhythmias, valvular and coronary diseases. More than 40 different inherited metabolic disorders can provoke cardiomyopathy, including lysosomal storage disorders, fatty acid oxidation defects, organic acidemias, amino acidopathies, glycogen storage diseases, congenital disorders of glycosylation as well as peroxisomal and mitochondrial disorders. If identified and diagnosed on time, some of congenital metabolic diseases could be successfully treated. It is important to assume them in cases when heart diseases are etiologically undefined. Rapid technological development has made it easier to establish the diagnosis of these diseases. This article will focus on common inherited metabolic disorders that cause heart diseases, as well as on diseases that might be possible to treat.

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COMMITTEE ON NUTRITION

PEDIATRICS ◽

10.1542/peds.40.2.289 ◽

1967 ◽

Vol 40 (2) ◽

pp. 289-304

Author(s):

CHARLES U. LOWE ◽

DAVID BAIRD COURSIN ◽

FELIX P. HEALD ◽

MALCOLM A. HOLLIDAY ◽

DONOUGH O'BRIEN ◽

...

Keyword(s):

Metabolic Disease ◽

Metabolic Diseases ◽

Dietary Treatment ◽

Nutritional Therapy ◽

The United States ◽

Detection Methods ◽

Dietary Therapy ◽

Treatment Practices ◽

Hereditary Metabolic Diseases ◽

Number Of Patients

THIRTEEN YEARS AGO a dietary approach to the therapy of phenylketonuria was proposed, and data on the usefulness as well as the very real limitations of this program have accumulated in the intervening years. At the present time studies on the application of special diets for use in this disease, as well as for many other hereditary metabolic diseases, are in progress. As wider use is made of procedures for detection of hereditary metabolic disease in the newborn, an increasingly larger number of patients who may benefit from appropriate nutritional therapy will be identified very early in life. For example, calculations based on the current birth rate and apparent incidence of phenylketonuria indicate that as many as 4,000 infants with this disorder in the United States alone could require dietary therapy in the next decade. There is, therefore, a need to evaluate the principles governing nutritional management of hereditary metabolic disease in order to develop optimal treatment facilities for use in conjunction with new detection methods. It seems anomalous that comparatively little has been done either to establish good treatment practices in hereditary metabolic disease or to mobilize scientific resources to ensure an optimistic out-come for therapeutic endeavors, while so much emphasis has been placed on detection. Dietary treatment of hereditary metabolic disease is simple in theory; however, practical application may be unexpectedly difficult, or even hazardous, if not carefully supervised. It should be determined whether: (1) the untreated disease is in fact harmful, (2) the treatment is useful in preventing or reversing the unfavorable progression of the disease, (3) the therapy may be harmful by interfering with growth or development, and (4) the program may be harmful to others to whom it is inadvertently or inappropriately given.

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Ayurveda Internal Medicine for the Management of Common Metabolic Disorders W.S.R. to Madhumeha and Sthoulya

Journal of Drug Delivery and Therapeutics ◽

10.22270/jddt.v9i5-s.3637 ◽

2019 ◽

Vol 9 (5-s) ◽

pp. 167-169

Author(s):

Dhananjay S. Khot

Keyword(s):

Internal Medicine ◽

Metabolic Syndrome ◽

Life Style ◽

Metabolic Disorders ◽

Dietary Habits ◽

Metabolic Diseases ◽

Health Issues ◽

The Metabolic Syndrome ◽

Sedentary Life Style

The metabolic disorders are major health issues of today’s scenario and incidences of metabolic diseases increases day by day due to the disturbed pattern of life style. Ayurveda texts have described term “Santarpanjanya Vikaras” which resembles diseases of defective tissue metabolism. Ayurveda mentioned that improper dietary habits and sedentary life style affects state of Agni which resulted Ama production and finally leading to the metabolic syndrome. The vitiation of Dosha, diminish state of Dhatu and blockage of channels, etc. also can initiate pathogenesis of metabolic disorders. The Kayachikitsa branch of Ayurveda recommended use of internal medicine for the management of various metabolic disorders. Considering increased health burden of society due to the metabolic syndrome present article explore role of ayurveda internal medicine for the management of metabolic syndrome. Keywords: Ayurveda, metabolic syndrome, Santarpanjanya, Madhumeha and Sthoulya.

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Genome-Wide DNA Methylation Profiles of Phlegm-Dampness Constitution

Cellular Physiology and Biochemistry ◽

10.1159/000487976 ◽

2018 ◽

Vol 45 (5) ◽

pp. 1999-2008 ◽

Cited By ~ 3

Author(s):

Haiqiang Yao ◽

Shanlan Mo ◽

Ji Wang ◽

Yingshuai Li ◽

Chong-Zhi Wang ◽

...

Keyword(s):

Dna Methylation ◽

Metabolic Disorders ◽

Mononuclear Cells ◽

Metabolic Diseases ◽

Body Type ◽

Peripheral Blood Mononuclear ◽

Molecular Features ◽

Genome Wide ◽

A Genome ◽

Differentially Methylated Genes

Background/Aims: Metabolic diseases are leading health concerns in today’s global society. In traditional Chinese medicine (TCM), one body type studied is the phlegm-dampness constitution (PC), which predisposes individuals to complex metabolic disorders. Genomic studies have revealed the potential metabolic disorders and the molecular features of PC. The role of epigenetics in the regulation of PC, however, is unknown. Methods: We analyzed a genome-wide DNA methylation in 12 volunteers using Illumina Infinium Human Methylation450 BeadChip on peripheral blood mononuclear cells (PBMCs). Eight volunteers had PC and 4 had balanced constitutions. Results: Methylation data indicated a genome-scale hyper-methylation pattern in PC. We located 288 differentially methylated probes (DMPs). A total of 256 genes were mapped, and some of these were metabolic-related. SQSTM1, DLGAP2 and DAB1 indicated diabetes mellitus; HOXC4 and SMPD3, obesity; and GRWD1 and ATP10A, insulin resistance. According to Ingenuity Pathway Analysis (IPA), differentially methylated genes were abundant in multiple metabolic pathways. Conclusion: Our results suggest the potential risk for metabolic disorders in individuals with PC. We also explain the clinical characteristics of PC with DNA methylation features.

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Hereditary Metabolic Diseases

Escourolle and Poirier's Manual of Basic Neuropathology ◽

10.1093/med/9780199929054.003.0010 ◽

2013 ◽

pp. 227-256

Author(s):

Frédéric Sedel ◽

Hans H. Goebel ◽

Douglas C. Anthony

Keyword(s):

Amino Acids ◽

Clinical Features ◽

Metabolic Disorders ◽

Metabolic Diseases ◽

The Other ◽

Structural Protein ◽

Cellular Organelle ◽

Biochemical Pathways ◽

Hereditary Metabolic Diseases ◽

Intermediate Metabolite

This chapter describes and illustrates the morphologic CNS changes in hereditary metabolic disorders. In some disorders, the metabolic derangements are most prominent in the cytosol and are linked to the dysfunction of a single cellular organelle. In these disorders there may be intracellular accumulation of an intermediate metabolite, resulting in a “storage disease” or accumulation of the abnormal substance within the cell. The organelles most commonly involved in these disorders are lysosomes, peroxisomes, mitochondria, and the cytoplasmic compartment. The other disorders are not linked to a specific cellular organelle. They are defined by an enzyme deficiency, the biochemical pathways involved (metabolic disorders of sugars, copper, amino acids, or structural protein), or only by morphologic/clinical features.

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Visfatin: A Possible Role in Cardiovasculo-Metabolic Disorders

Cells ◽

10.3390/cells9112444 ◽

2020 ◽

Vol 9 (11) ◽

pp. 2444

Author(s):

Ali Dakroub ◽

Suzanne A. Nasser ◽

Nour Younis ◽

Humna Bhagani ◽

Yusra Al-Dhaheri ◽

...

Keyword(s):

Nicotinamide Adenine Dinucleotide ◽

Intracellular Signaling ◽

Skeletal Muscles ◽

Metabolic Disorders ◽

Metabolic Diseases ◽

Signaling Cascades ◽

Nicotinamide Phosphoribosyltransferase ◽

Enhancing Factor ◽

Cell Colony

Visfatin/NAMPT (nicotinamide phosphoribosyltransferase) is an adipocytokine with several intriguing properties. It was first identified as pre-B-cell colony-enhancing factor but turned out to possess enzymatic functions in nicotinamide adenine dinucleotide biosynthesis, with ubiquitous expression in skeletal muscles, liver, cardiomyocytes, and brain cells. Visfatin exists in an intracellular (iNAMPT) and extracellular (eNAMPT) form. Intracellularly, visfatin/iNAMPT plays a regulatory role in NAD+ biosynthesis and thereby affects many NAD-dependent proteins such as sirtuins, PARPs, MARTs and CD38/157. Extracellularly, visfatin is associated with many hormone-like signaling pathways and activates some intracellular signaling cascades. Importantly, eNAMPT has been associated with several metabolic disorders including obesity and type 1 and 2 diabetes. In this review, a brief overview about visfatin is presented with special emphasis on its relevance to metabolic diseases. Visfatin/NAMPT appears to be a unique molecule with clinical significance with a prospective promising diagnostic, prognostic, and therapeutic applications in many cardiovasculo-metabolic disorders.

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Molecular Insight into the Interaction between Epigenetics and Leptin in Metabolic Disorders

Nutrients ◽

10.3390/nu11081872 ◽

2019 ◽

Vol 11 (8) ◽

pp. 1872 ◽

Cited By ~ 6

Author(s):

Adam Wróblewski ◽

Justyna Strycharz ◽

Ewa Świderska ◽

Karolina Drewniak ◽

Józef Drzewoski ◽

...

Keyword(s):

Metabolic Syndrome ◽

Histone Deacetylases ◽

Metabolic Disorders ◽

Metabolic Diseases ◽

Current Knowledge ◽

Epigenetic Modifications ◽

Leptin Sensitivity ◽

Epigenetic Machinery ◽

Biological Event ◽

Plasma Leptin

Nowadays, it is well-known that the deregulation of epigenetic machinery is a common biological event leading to the development and progression of metabolic disorders. Moreover, the expression level and actions of leptin, a vast adipocytokine regulating energy metabolism, appear to be strongly associated with epigenetics. Therefore, the aim of this review was to summarize the current knowledge of the epigenetic regulation of leptin as well as the leptin-induced epigenetic modifications in metabolic disorders and associated phenomena. The collected data indicated that the deregulation of leptin expression and secretion that occurs during the course of metabolic diseases is underlain by a variation in the level of promoter methylation, the occurrence of histone modifications, along with miRNA interference. Furthermore, leptin was proven to epigenetically regulate several miRNAs and affect the activity of the histone deacetylases. These epigenetic modifications were observed in obesity, gestational diabetes, metabolic syndrome and concerned various molecular processes like glucose metabolism, insulin sensitivity, liver fibrosis, obesity-related carcinogenesis, adipogenesis or fetal/early postnatal programming. Moreover, the circulating miRNA profiles were associated with the plasma leptin level in metabolic syndrome, and miRNAs were found to be involved in hypothalamic leptin sensitivity. In summary, the evidence suggests that leptin is both a target and a mediator of epigenetic changes that develop in numerous tissues during metabolic disorders.

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Disrupting phosphatase SHP2 in macrophages protects mice from high-fat diet-induced hepatic steatosis and insulin resistance by elevating IL-18 levels

Journal of Biological Chemistry ◽

10.1074/jbc.ra119.011840 ◽

2020 ◽

Vol 295 (31) ◽

pp. 10842-10856 ◽

Cited By ~ 1

Author(s):

Wen Liu ◽

Ye Yin ◽

Meijing Wang ◽

Ting Fan ◽

Yuyu Zhu ◽

...

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Hepatic Steatosis ◽

High Fat Diet ◽

Metabolic Disorders ◽

Metabolic Diseases ◽

Low Grade ◽

High Fat ◽

Caspase 1

Chronic low-grade inflammation plays an important role in the pathogenesis of type 2 diabetes. Src homology 2 domain-containing tyrosine phosphatase-2 (SHP2) has been reported to play diverse roles in different tissues during the development of metabolic disorders. We previously reported that SHP2 inhibition in macrophages results in increased cytokine production. Here, we investigated the association between SHP2 inhibition in macrophages and the development of metabolic diseases. Unexpectedly, we found that mice with a conditional SHP2 knockout in macrophages (cSHP2-KO) have ameliorated metabolic disorders. cSHP2-KO mice fed a high-fat diet (HFD) gained less body weight and exhibited decreased hepatic steatosis, as well as improved glucose intolerance and insulin sensitivity, compared with HFD-fed WT littermates. Further experiments revealed that SHP2 deficiency leads to hyperactivation of caspase-1 and subsequent elevation of interleukin 18 (IL-18) levels, both in vivo and in vitro. Of note, IL-18 neutralization and caspase-1 knockout reversed the amelioration of hepatic steatosis and insulin resistance observed in the cSHP2-KO mice. Administration of two specific SHP2 inhibitors, SHP099 and Phps1, improved HFD-induced hepatic steatosis and insulin resistance. Our findings provide detailed insights into the role of macrophagic SHP2 in metabolic disorders. We conclude that pharmacological inhibition of SHP2 may represent a therapeutic strategy for the management of type 2 diabetes.

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Saturated hydrogen improves lipid metabolism disorders and dysbacteriosis induced by a high-fat diet

Experimental Biology and Medicine ◽

10.1177/1535370219898407 ◽

2020 ◽

Vol 245 (6) ◽

pp. 512-521 ◽

Cited By ~ 5

Author(s):

Xiangjie Qiu ◽

Qiaona Ye ◽

Mengxing Sun ◽

Lili Wang ◽

Yurong Tan ◽

...

Keyword(s):

Fatty Acid ◽

High Fat Diet ◽

Metabolic Disorders ◽

Metabolic Diseases ◽

Isocitrate Lyase ◽

Intestinal Flora ◽

Glyoxylic Acid ◽

Density Lipoprotein ◽

High Fat ◽

Acid Cycle

Studies have shown that metabolic diseases, such as obesity, are significantly associated with intestinal flora imbalance. The amplification of opportunistic pathogens induced by the glyoxylic acid cycle contributes to intestinal flora imbalance. Promising, though, is that saturated hydrogen can effectively improve the occurrence and development of metabolic diseases, such as obesity. However, the specific mechanism of how saturated hydrogen operates is still not very clear. In this study, after a high-fat diet, the level of total cholesterol, total glyceride, and low-density lipoprotein in the peripheral blood of mice increased, and that of high-density lipoprotein decreased. Intestinal fatty acid metabolism-related gene Apolipoprotein E (ApoE), fatty acid synthase (FAS), intestinal fatty acid-binding protein (I-FAPB), acetyl-CoA carboxylase 1 (ACC1), peroxisome proliferator-activated receptor γ (PPARγ), and stearoyl-CoA desaturase 1 (SCD1) increased significantly. Bacteroides, Bifidobacteria, and Lactobacillus counts in feces decreased considerably, while Enterobacter cloacae increased. The activity of isocitrate lyase in feces increased markedly. Treatment of mice with saturated hydrogen led to decreased total cholesterol, total glyceride, and low-density lipoprotein and increased high-density lipoprotein in the peripheral blood. FAS and I-FAPB gene expression in the small intestine decreased. Bacteroides, Bifidobacteria, and Lactobacillus in feces increased significantly, whereas Enterobacter cloacae decreased. The activity of isocitrate lyase also diminished remarkably. These results suggest that saturated hydrogen could improve intestinal structural integrity and lipid metabolism disorders by inhibiting the glyoxylic acid cycle of the intestinal flora. Impact statement Past studies have shown that hydrogen can improve metabolic disorders, but its mechanism of action remains unclear. It is well known that metabolic diseases, such as obesity, are significantly associated with changes in the intestinal flora. The glyoxylic acid cycle is an essential metabolic pathway in prokaryotes, lower eukaryotes, and plants and could be the portal for mechanisms related to metabolic disorders. Many opportunistic pathogenic bacteria can recycle fatty acids to synthesize sugars and other pathogenic substances using the glyoxylic acid cycle. So, the glyoxylic acid cycle may be involved in intestinal dysbacteriosis under high-fat diet. This study, therefore, seeks to provide the mechanism of how hydrogen improves metabolic diseases and a new basis for the use of hydrogen in the treatment of metabolic disorders.

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