Metabolic Syndrome Comorbidities Research Articles

Comparative Analysis of the Quality of Life Scales Parameters in Patients with Combination of Stable Ischemic Heart Disease and Metabolic Syndrome

Modern epidemiological studies confirm that comorbid diseases and conditions can have significant impact on diagnostic and treatment of the underlying disease. The problem of the comorbidy of stable coronary heart disease (SCHD) and metabolic syndrome (MS) has high medical and social significance, need high costs for diagnosis and treatment, and leads to decreased of quality of life (QOL). QOL is an important indicator of the health status of patients, which comprehensively characterizes human physical, psychological, emotional and social functioning. The objective: to conduct a comparative analysis of the QOL of patients with combination of SCAD and MS versus patients with isolated SCHD. Materials and methods. The study included 102 patients: 52 people with MS in combination with SCAD and 50 patients with SCHD only. There were 42 (51.2%) men (mean age 49.8 ± 5.3 years), and 40 (48.8%) women (mean age 51.6 ± 6.7 years). The QoL score was assessed by general medical questionnaire – the Medical Outcomes Study 36-Item (SF-36), in which all scales form two indicators: mental and physical health and a specialized questionnaire for patient with stable angina pectoris – SAQ (Seattle Angina Questionnaire). The diagnosis of SCHD with functional class (FC) assessment was performed by European Society of Cardiology criteria. MS was established if three out of five diagnostic criteria were met. Results. Patients with comorbid MS and SCHD demonstrated significantly lower QoL scores, both in psychological and physical components of health (according to the SF-36 questionnaire) compared to patients with SCHD alone (p <0.05). An analysis of the SAQ questionnaire data also showed significantly lower points in group of patients with NAS and SCHD combination compared to the group of patients with isolated SCHD (in total, by 8.76%; p <0.05). Conclusion. Patients with metabolic syndrome in combination with stable coronary heart disease (SCHD) had a statistically significantly lower level of quality of life according to the evaluation by both SF-36 nonspecific questionnaire and the SAQ specific questionnaire comparing to group of patients with isolated SCAD.

Оптимизация вторичной профилактики переломов костей при остеопорозе у менопаузальных женщин и роль коморбидного метаболического синдрома

Актуальность. Остеопороз (ОП) характеризуется хрупкостью скелета и подверженностью людей переломам, обусловленным уменьшением костной массы и ухудшением микроархитектуры кости. У неменструирующих женщин ломкость костей более выражена, а остеопоротические переломы встречаются втрое чаще. Ухудшает течение ОП у менопаузальных женщин наличие коморбидного метаболического синдрома (МС) и его тяжесть, что требует совершенствования лечебных мероприятий у таких больных. Цель исследования: повысить эффективность лечения ОП у менопаузальных женщин с МС и качество вторичной профилактики у них костных переломов. Материалы и методы. В течение двух лет под наблюдением находились 28 неменструирующих женщин с ОП в возрасте от 37 до 72 лет (в среднем 50 лет). Во всех случаях наступила физиологическая менопауза. Минеральную плотность кости оценивали по Т-индексу остеоденситограмм, рентгенологическим индексам Барнетта — Нордина, Рохлина и клиновидности. В сыворотке крови исследовали показатели, которые отражали состояние костного метаболизма и МС. ­Результаты. У менопаузальных женщин, страдающих ОП, переломы бедренной кости, позвоночника, костей запястья и ІІ плюсневой диагностированы в 39 % случаев. Остеофрактуры были прямо связаны с возрастом больных, параметром остеоденситометрического индекса, наличием и тяжестью течения коморбидного МС, составляющих его факторов (IV типа гиперлипидемии и сахарного диабета второго типа), с наличием диабетической нейропатии, а также с исходными концентрациями в крови Mg, Mn, Pb и Se. Разработана оптимальная вторичная профилактика костных переломов у менопаузальных женщин с коморбидными ОП и МС, основанная на индивидуальных подходах к длительному назначению препаратов Са, Se, Zn, бисфосфонатов, ранелата Sr, фибратов и урикодепрессоров с учетом характера и тяжести течения МС. Выводы. Предложенная медицинская технология лечения ОП у неменструирующих женщин с МС позволила сократить число остеофрактур в 10 раз, уменьшить активность в крови щелочной фосфатазы и показатель остеоденситометрического индекса.

Chastota porushen rytmu i providnosti ta antyarytmichna efektyvnist upstream-terapii u khvorykh na hostryi infarkt miokarda z komorbidnymy metabolichnym syndromom i endotelialnoiu dysfunktsiieiu sudyn

Context. Cardiac arrhythmias and conduction disorders are the most common reperfusion complications in patients with myocardial infarction (MI) in both acute and late postinfarction periods, which significantly complicates the course of the disease and often leads to an unfavorable prognosis for the early and distant periods. Objective. To evaluate the frequency of arrhythmias and conduction and the antiarrhythmic efficacy of upstream therapy in patients with acute MI with comorbid metabolic syndrome (MS) and endothelial vascular dysfunction. Materials and methods. The experimental group consisted of 42 patients with acute myocardial infarction in combination with MS, who underwent urgent coronary angiography followed by balloon angioplasty and stenting of the infarct-dependent coronary artery, as well as standard drug therapy according to the MOH protocol. Patients in the experimental group also received 5 intravenous infusions of arginine-carnitine mixture (4.2 g and 2.0 g, respectively) in 100 ml of solvent. The nature of the clinical course of MI was compared with that in 38 patients with MI in combination with MS (control group), who did not receive additional treatment and were comparable in age (56.64 ± 0.91 and 54.85 ± 0.76 years, respectively). Results. It was found that patients with MI with comorbid MS on percutaneous coronary intervention most often developed reperfusion syndrome with manifestations of arrhythmias and conduction. Under the influence of standard drug treatment in patients of the control group there was a significant clinical and functional improvement, though sinus tachycardia, ventricular extrasystole of high grades and supraventricular extrasystole remained resistant to treatment. There was also a pronounced endothelial vascular dysfunction, which in the process of standard treatment in patients of the control group did not reach the level of healthy individuals (p-value less than 0.05). Conclusions. In patients with acute MI with comorbid MS, who underwent balloon angioplasty and stenting of the infarct-dependent coronary artery, a pronounced vascular endothelial dysfunction and electrical instability is observed, accompanied by reperfusion arrhythmias and arrhythmias. The use of arginine-carnitine mixture as upstream therapy helped to restore endothelial function and showed a pronounced antiarrhythmic effect, which significantly reduced the incidence and severity of complications of acute MI such as reperfusion arrhythmias.

Chronic stress induced perivascular adipose tissue impairment of aortic function and the therapeutic effect of exercise.

What is the central question of this study? Thoracic perivascular adipose tissue (tPVAT) is known to, in part, regulate aortic function: what are the effects of unpredictable chronic mild stress (UCMS) on the tPVAT regulation of aortic function and what is the role of exercise training in alleviating the potential negative actions of UCMS on tPVAT? What is the main finding and its importance? UCMS causes tPVAT to disrupt endothelium-dependent dilatation, increases inflammatory cytokine production and diminishes tPVAT-adiponectin. Exercise training proved efficacious in preventing tPVAT-mediated disruption of aortic function. The data support a tPVAT mechanism through which chronic stress negatively impacts vascular health, which adds to our knowledge of how psychological disorders might increase the risk of cardiovascular disease. Chronic stress is a major risk for cardiovascular disease. Perivascular adipose tissue (PVAT) has been shown to regulate vascular function; however, the impact of chronic stress and the comorbidity of metabolic syndrome (MetS) on thoracic (t)PVAT is unknown. Additionally, aerobic exercise training (AET) is known to combat the pathology of MetS and chronic stress, but the role of tPVAT in these actions is also unknown. Therefore, the purpose of this study was to examine the effects of unpredictable chronic mild stress (UCMS) on the tPVAT regulation of aortic function and the preventative effect of AET. Lean (LZR) and obese (OZR) Zucker rats (16-17weeks old) were exposed to 8weeks of UCMS with and without treadmill exercise (AET). In LZR, UCMS impaired aortic endothelium-dependent dilatation (EDD) (assessed ex vivo by wire myography) and aortic stiffness (assessed by elastic modulus) with no change in OZR subject to UCMS. However, both LZR and OZR UCMS tPVAT impaired EDD compared to respective controls. LZR and OZR subject to UCMS had higher oxidative stress production, diminished adiponectin and impaired aortic nitric oxide levels. Divergently, UCMS induced greater inflammatory cytokine production in LZR UCMS tPVAT, but not in OZR UCMS tPVAT. AET prevented the tPVAT impairment of aortic relaxation with UCMS in LZR and OZR. Additionally, AET reduced aortic stiffness in both LZR and OZR. These beneficial effects on tPVAT regulation of the aorta are likely due to AET preservation of adiponectin, reduced oxidative stress and inflammation, and enhanced nitric oxide. UCMS impaired tPVAT-regulated aortic function in LZR, and augmented MetS-induced EDD in OZR. Conversely, AET in combination with UCMS largely preserved aortic function and the tPVAT environment, in both groups.

Obesity-prone rats fed with high-fat diet as a model of HFpEF

Heart failure with preserved ejection fraction (HFpEF) is a common and complex syndrome with high mortality and morbidity rates for which there are currently no evidence-based therapies. As patients with HFpEF very often harbor comorbidities of metabolic syndrome, we hypothesized, that metabolic syndrome in aging animals could be a major mechanism underlying the development of diastolic dysfunction and HFpEF. Therfeore, obesity-prone (OP) and -resistant (OR) rats were respectively fed with a high-fat diet (HFD) or a standard rat chow (Std) for 4 months or for 12 months ( n = 10 rats in each group; 4 groups). At the end of the protocol, abdominal obesity, complete phenotyping of metabolic syndrome, associated to echocardiographic and left and right ventricular catheterization measurements, were performed. Blood was sampled before euthanasia of the animals. After 4- and 12-month HFD, OP rats presented increased total body and abdominal fat weights, altered glucose tolerance test and dyslipidemia. In OP rats, left ventricular systolic (164 ± 6 versus 120 ± 5 mmHg, P < 0.001) and end-diastolic pressures (1.9 ± 0.3 versus 9.2 ± 1.9 mmHg, P < 0.05) increased after 12-month HFD, while there were unchanged after 4 months. Echocardiography showed increased left ventricular mass and relative surface area in 12-month HFD-fed OP rats, together with preserved ejection fraction (around 65%). Right ventricular systolic pressure was increased in 12-month HFD-fed OP rats (31.1 ± 0.8 versus 26.7 ± 0.4 mmHg, P < 0.01). In addition, circulating NT-proBNP levels were decreased compared to OR rats, while ST2 levels increased. Metabolic syndrome induced by 12-month HFD in OP rats leads to the development of HFpEF. In these rats, circulating NT-proBNP levels were decreased, while circulating ST2 levels were largely increased.

PREVALENCE AND TIME OF DEVELOPMENT OF SYSTEMIC ARTERIAL HYPERTENSION IN PATIENTS AFTER LIVER TRANSPLANTATION.

The use of immunosuppressive drugs after liver transplantation (LT) is associated with the development of systemic arterial hypertension (SAH), in addition to other comorbidities of metabolic syndrome. Therefore, the purpose of this study was to analyze the time after use immunosuppressive drugs the patient progresses to SAH, as well as to identify its prevalence and the factors that may be correlated to it. A retrospective and longitudinal study was conducted, based on the analysis of medical records of 72 normotensive patients, attended in the transplant unit of a university hospital, between 2016 and 2019. It was observed, on average, 9±6.98 months after immunosuppressive use, the patients were diagnosed with hypertension, and the prevalence of transplanted patients who evolved to SAH in this study was 59.64% (41 patients). In addition, there was a correlation between serum dosage of tacrolimus and the development of SAH (P=0.0067), which shows that tacrolimus has a significant role in the development of SAH. Finally, it was noticed that the development of post-transplantation hypertension indicates a higher risk of the patient presenting the other parameters of metabolic syndrome, as well as a higher impairment in its renal function (P=0.0061). This study shows that the patients evolved to SAH in an average of 9±6.98 months after immunosuppressive drug use. We have also found high prevalence of systemic arterial hypertension (59.64%) in patients after liver transplantation, who used calcineurin inhibitors, especially when associated with the use of tacrolimus.

Brown Seaweeds for the Management of Metabolic Syndrome and Associated Diseases.

Metabolic syndrome is characterized by the coexistence of different metabolic disorders which increase the risk of developing type 2 diabetes mellitus and cardiovascular diseases. Therefore, metabolic syndrome leads to a reduction in patients’ quality of life as well as to an increase in morbidity and mortality. In the last few decades, it has been demonstrated that seaweeds exert multiple beneficial effects by virtue of their micro- and macronutrient content, which could help in the management of cardiovascular and metabolic diseases. This review aims to provide an updated overview on the potential of brown seaweeds for the prevention and management of metabolic syndrome and its associated diseases, based on the most recent evidence obtained from in vitro and in vivo preclinical and clinical studies. Owing to their great potential for health benefits, brown seaweeds are successfully used in some nutraceuticals and functional foods for treating metabolic syndrome comorbidities. However, some issues still need to be tackled and deepened to improve the knowledge of their ADME/Tox profile in humans, in particular by finding validated indexes of their absorption and obtaining reliable information on their efficacy and long-term safety.

Excess serum uric acid is associated with metabolic syndrome in obese adolescent patients

PurposeObesity is a significant cause of morbidity in adolescents. Excess serum uric acid (SUA) has been associated with metabolic syndrome (MS) among adults. We evaluated the relationship among SUA and markers of insulin resistance (IR) and low-grade inflammation in obese adolescents with and without MS.MethodsThe study was a retrospective chart review of obese patients seen in the LeBonheur Endocrine clinic seen in clinic between September 2016 and December 2017. MS was defined as according to the International Diabetes Federation. Body mass index standard deviation score (BMI SDS), systolic blood pressure (SBP), diastolic blood pressure (DBP), body composition, fasting lipids, glucose, high sensitivity c-reactive protein (hs-CRP), serum uric acid (SUA), HbA1c, alanine transferase (ALT), aspartate transferase (AST), insulin and homeostatic model assessment for insulin resistance (HOMA-IR) were extracted from the charts of the 100 obese adolescents (57% female).ResultsHyperuricemia (SUA >357 umol/L) was present in 41.8% of entire cohort without significant ethnic/racial and/or gender differences. Adolescents with HUA had higher FM, SBP, HbA1c, insulin and HOMA-IR (p < 0.05). While SUA was positively correlated with FM, SBP, HOMA-IR and HbA1c, and triglyceride:HDL-C ratio (TG:HDL-C) (p < 0.05). MS was identified in 32.8% of cohort. MS showed significantly higher FM, SBP, DBP, SUA, ALT, insulin, HOMA-IR, and TG:HDL-c ratio than non-MS subgroup (p < 0.05). FM was positively correlated with SUA, HOMA-IR and hsCRP (p < 0.01).ConclusionsIn our study, those with hyperuricemia (HUA) showed elevated markers of metabolic syndrome including BP, serum glucoses, IR and triglycerides. In our cohort, SUA appears to correlate with MS comorbidities.

Consequences of maternal bariatric surgery: potential for reduced amino acid availability to the fetus

Though bariatric surgery is the most effect method of durable weight loss, it is not understood why or how it works so effectively to reduce the comorbidities of Metabolic Syndrome. Both in humans and rodents, maternal bariatric surgery prior to pregnancy results in challenges during pregnancy including increased small‐for‐gestational age offspring and greater risk for fetal demise. We have shown in the rodent model of vertical sleeve gastrectomy (VSG) that offspring develop greater risk for metabolic disease later in life compared to obese controls. A common gestational cause of poor growth in utero is maternal protein deficiency. In the current work, we hypothesize that the transporters within the placenta may be differentially transporting amino acids to the fetus despite previously demonstrating that protein levels in the VSG dam were not harmed by surgery and were sufficient to sustain a health pregnancy. Using gestational day 19 placenta from pregnant Lean, Obese and post‐VSG dams, we performed analysis of the amino acid content of the placenta and prepared placental mRNA for quantitative PCR analysis of genes associated with amino acid transport. Aliphatic amino acids: isoleucine, leucine, proline and valine were significantly reduced in comparison to Lean dam levels (p&lt; 0.05). Phenylalanine, aspartic acid and glutamic acid, arginine, histidine and methionine were also significantly reduced (p&lt; 0.05). Furthermore, amino acid transporter SLC38A1 (SNAT1) and SLC38A4 (SNAT4) showed trends towards reductions in both VSG and Obese dams. On the contrary, SLC38A2 (SNAT2) and SLC7a7 (LAT1) was significantly elevated (p&lt; 0.05) in VSG in comparison to Lean and Obese. This affect appeared specific to amino acids since carbohydrate transporters remained unchanged. Collectively, these data suggest that despite healthy ingestion of proteins by the VSG dam, alterations in amino acid availability to the fetus may be obstructed by the placenta after bariatric surgery. This reduced level of amino acid availability may contribute to poor outcomes in bariatric pregnancy. More work is needed to determine the relevance of these findings to humans.Support or Funding InformationResearch was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number P20GM104357 and P20GM121334.

The Vascular Consequences of Metabolic Syndrome: Rodent Models, Endothelial Dysfunction, and Current Therapies.

Metabolic syndrome is characterized by visceral obesity, dyslipidemia, hyperglycemia and hypertension, and affects over one billion people. Independently, the components of metabolic syndrome each have the potential to affect the endothelium to cause vascular dysfunction and disrupt vascular homeostasis. Rodent models of metabolic syndrome have significantly advanced our understanding of this multifactorial condition. In this mini-review we compare the currently available rodent models of metabolic syndrome and consider their limitations. We also discuss the numerous mechanisms by which metabolic abnormalities cause endothelial dysfunction and highlight some common pathophysiologies including reduced nitric oxide production, increased reactive oxygen species and increased production of vasoconstrictors. Additionally, we explore some of the current therapeutics for the comorbidities of metabolic syndrome and consider how these benefit the vasculature.

White matter inflammation and cognitive function in a co-morbid metabolic syndrome and prodromal Alzheimer\u2019s disease rat model

BackgroundMetabolic syndrome, the development of which is associated with high-caloric Western diet (HCD) intake, represent a risk factor for mild cognitive impairment (MCI) and dementia including Alzheimer’s disease (AD) later in life. This study aimed to investigate the effect of diet-induced metabolic disturbances on white matter neuroinflammation and cognitive function in a transgenic (TG) Fischer 344 rat carrying a human β-amyloid precursor protein (APP) gene with Swedish and Indiana mutations (APP21 TG), a model of pre-AD and MCI.MethodsTG and wildtype (WT) rats received either a HCD with 40% kJ from fat supplemented with 20% corn syrup drink or a standard diet for 12 weeks. Body weight, caloric intake, and blood pressure were measured repeatedly. End-point changes in glucose and lipid metabolism were also assessed. Open field task was used for assessment of activity; Morris water maze was used to assess spatial learning and memory. Cerebral white matter microglia and astrocytes, hippocampal neurons, and neuronal synapses were examined using immunohistochemistry.ResultsRats maintained on the HCD developed significant obesity, visceral adiposity, dyslipidemia, and hyperinsulinemia, but did not become hypertensive. Impaired glucose tolerance was observed only in WT rats on the HCD. Total microglia number, activated OX-6+ microglia, as well as GFAP+ astrocytes located predominantly in the white matter were greater in the APP21 TG rat model in comparison to WT rats. HCD-driven metabolic perturbations further exacerbated white matter microgliosis and microglia cell activation in the APP21 TG rats and led to detectable changes in spatial reference memory in the comorbid prodromal AD and metabolic syndrome group compared to WT control rats. Neuronal density in the CA1 subregion of the hippocampus was not different between the experimental groups. Synaptic density in the CA1 and CA3 hippocampal subregions was lower in the TG rats compared to WT rats; however, there was no additional effect of the co-morbidity on this measure.ConclusionsThese results suggest that white matter neuroinflammation might be one of the possible processes of early interaction of metabolic syndrome with MCI and pre-AD and could be one of the early brain pathologies contributing to cognitive deficits observed in mild cognitive impairment and dementia, including AD cases.

The vagus nerve and the sympathetic nervous system act in concert to modulate immunity

Metabolic syndrome represents a major risk factor for severe comorbidities such as cardiovascular diseases or diabetes. It is also associated with an increased prevalence of emotional and cognitive alterations that in turn aggravate the disease and related outcomes. Identifying therapeutic strategies able to improve those alterations is therefore a major socioeconomical and public health challenge. We previously reported that both hippocampal inflammatory processes and neuronal plasticity contribute to the development of emotional and cognitive alterations in db/db mice, an experimental model of metabolic syndrome that displays most of the classical features of the syndrome. In that context, nutritional interventions with known impact on those neurobiological processes appear as a promising alternative to limit the development of neurobiological comorbidities of metabolic syndrome. We therefore tested here whether n-3 polyunsaturated fatty acids (n-3 PUFAs) associated with a cocktail of antioxidants can protect against the development of behavioral alterations that accompany the metabolic syndrome. Thus, this study aimed: 1) to evaluate if a diet supplemented with the plant-derived n-3 PUFA α-linolenic acid (ALA) and antioxidants (provided by n-3 PUFAs-rich rapeseed oil fortified with a mix of naturally constituting antioxidant micronutrients, including coenzyme Q10, tocopherol, and the phenolic compound canolol) improved behavioral alterations in db/db mice, and 2) to decipher the biological mechanisms underlying this behavioral effect. Although the supplemented diet did not improve anxiety-like behavior and inflammatory abnormalities, it reversed hippocampus-dependent spatial memory deficits displayed by db/db mice in a water maze task. It concomitantly changed subunit composition of glutamatergic AMPA and NMDA receptors in the hippocampus that has been shown to modulate synaptic function related to spatial memory. These data suggest that changes in local neuronal plasticity may underlie cognitive improvements in db/db mice fed the supplemented diet. The current findings might therefore provide valuable data for introducing new nutritional strategies for the treatment of behavioral complications associated with MetS.

Prevalence of non-alcoholic fatty liver and liver fibrosis in patients with moderate-severe psoriasis: A cross-sectional cohort study.

Several studies have reported that non-alcoholic fatty liver disease (NAFLD) is more frequent in patients with psoriasis, but few have reviewed the presence of liver fibrosis in those patients. Cross-sectional cohort, single-centre study, continuously selecting all patients with moderate-severe psoriasis seen at the Psoriasis Unit of a Tertiary Hospital. The grade of liver steatosis was assessed using liver ultrasound, and the quantity of liver fibrosis was graded using a transitional vibration-controlled elastography (Fibroscan®). A total of 71 patients (66.2% male)were included, with an average age of 46.6years old. The maximum historical PASI average was 14.4 while the baseline PASI average at the time of the study was 2. A third (36%) of patients met the criteria for metabolic syndrome 52% of patients had steatosis; being male, having metabolic syndrome comorbidities, elevated AST/ALT enzymes, dyslipidemia and high initial PASI were significantly related. 14% of patients had moderate liver fibrosis (≥7.6 KPa). In 30% of them, no ultrasound liver steatosis was observed. Elastography may be a useful tool along with ultrasound to evaluate liver disease in patients with psoriasis.

Rapeseed oil fortified with micronutrients improves cognitive alterations associated with metabolic syndrome

Metabolic syndrome represents a major risk factor for severe comorbidities such as cardiovascular diseases or diabetes. It is also associated with an increased prevalence of emotional and cognitive alterations that in turn aggravate the disease and related outcomes. Identifying therapeutic strategies able to improve those alterations is therefore a major socioeconomical and public health challenge. We previously reported that both hippocampal inflammatory processes and neuronal plasticity contribute to the development of emotional and cognitive alterations in db/db mice, an experimental model of metabolic syndrome that displays most of the classical features of the syndrome. In that context, nutritional interventions with known impact on those neurobiological processes appear as a promising alternative to limit the development of neurobiological comorbidities of metabolic syndrome. We therefore tested here whether n-3 polyunsaturated fatty acids (n-3 PUFAs) associated with a cocktail of antioxidants can protect against the development of behavioral alterations that accompany the metabolic syndrome. Thus, this study aimed: 1) to evaluate if a diet supplemented with the plant-derived n-3 PUFA α-linolenic acid (ALA) and antioxidants (provided by n-3 PUFAs-rich rapeseed oil fortified with a mix of naturally constituting antioxidant micronutrients, including coenzyme Q10, tocopherol, and the phenolic compound canolol) improved behavioral alterations in db/db mice, and 2) to decipher the biological mechanisms underlying this behavioral effect. Although the supplemented diet did not improve anxiety-like behavior and inflammatory abnormalities, it reversed hippocampus-dependent spatial memory deficits displayed by db/db mice in a water maze task. It concomitantly changed subunit composition of glutamatergic AMPA and NMDA receptors in the hippocampus that has been shown to modulate synaptic function related to spatial memory. These data suggest that changes in local neuronal plasticity may underlie cognitive improvements in db/db mice fed the supplemented diet. The current findings might therefore provide valuable data for introducing new nutritional strategies for the treatment of behavioral complications associated with MetS.

MODERN APPROACH TOWARDS THE TREATMENT OF COMORBID PATHOLOGY

Osteoarthritis (OA) is a common, poly-etiological disease of the joints, the occurrence and development of which is associated with a number of genetic, endogenous (hormonal balance, immune disorders, oxidative stress) and exogenous factors (trauma, overload). The combination of metabolic syndrome (MS) and OA is one of the most pressing medical and social issues for healthcare today. This is due to both their extremely high prevalence and high comorbidity with other conditions and diseases that have a significant impact on the quality of life of patients. The aim of our work was to study the pleurotropic effect of rosuvastatin on the pain intense and disease intensity in the course of OA in patients with comorbid MS, as well as its effect on blood pressure (BP), heart rate (HR), level of anthropometric indicators and lipidogram indicators. 30 patients were examined for OA and MS. Patients were divided into two age-matched groups. Rosuvastatin was prescribed to group I (n = 15) in a dose of 20 mg once a day for 12 days. The criteria for assessing the therapy efficacy included pain severity, articular and anthropometric parameters, laboratory and instrumental parameters, the level of quality of life. Patients were examined twice: before the therapy and on the day 12 of the therapy. It has been established that the rozuvastatin prescribed for this category of patients can reduce pain, improve joint function, lower the intensity of the disease and improve the quality of life of patients. In addition, rozustastatin does not affect the level of systolic and diastolic blood pressure, and can be prescribed for patients with concomitant arterial hypertension.

Reduced amino acids: the placenta after maternal vertical sleeve gastrectomy in the rat

Vertical sleeve gastrectomy (VSG) is a surgical weight loss procedure used to reduce the comorbidities of Metabolic Syndrome improving obesity, diabetes and heart disease. Both in humans and rodents, maternal bariatric surgery prior to pregnancy results in challenges during pregnancy including increased small‐for‐gestational age offspring that we have shown in the rodent model of VSG develop greater metabolic disease later in life compared to obese controls. A common gestational cause of poor growth in utero is maternal protein deficiency. Previously, we published that VSG dams had normal levels of plasma amino acids in the fasting condition and following a protein shake gavage. We did not find any gross abnormalities in plasma amino acids under these conditions. In the current work, we hypothesized that the maternal levels were sufficient and that the transporters within the placenta may be differentially transporting amino acids to the fetus. Using gestational day 19 placenta from pregnant Lean, Obese and post‐VSG dams, we performed analysis of the amino acid content of the placenta and prepared placental mRNA for quantitative PCR analysis of genes associated with amino acid transport. Aliphatic Amino acids: isoleucine, leucine, proline and valine were statistically reduced in comparison to Lean dam levels (p&lt; 0.05). Phenylalanine, aspartic acid and glutamic acid, arginine, histidine and methionine were also significantly reduced (p&lt; 0.05). Furthermore, amino acid transporter SLC38A1 (SNAT1) and SLC38A4 (SNAT4) showed trends towards reductions in both VSG and Obese dams. On the contrary, SLC38A2 (SNAT2) and SLC7a7 (LAT1) was significantly elevated (p&lt; 0.05) in VSG in comparison to Lean and Obese. Collectively, these data suggest that despite healthy ingestion of proteins by the mother, alterations in amino acid availability to the fetus may be obstructed by the placenta after bariatric surgery. More work is needed in order to determine the relevance of these findings to the human condition.Support or Funding InformationThe research reported in this publication was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number 1P20GM121334‐01, and BEG is also supported DOD contract W81XWH‐16‐1‐0387.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

APOE ε4, the door to insulin-resistant dyslipidemia and brain fog? A case study

For decades, scientists have known that carriers of the apolipoprotein E ε4 (APOE ε4) allele (homozygous/heterozygous) are at respectively higher risk for developing Alzheimer's disease (AD). Although previous research reveals that the APOE ε4 variant impacts the clearance capacity and degradation of β-amyloid from the brain, as compared with APOE ε3 (wild type with normal risk) and APOE ε2 (variant with accelerated clearance and reduced risk), little has been documented about APOE ε4's dual role in cholesterol transport, both peripheral and cerebral, and the effects of sluggish APOE ε4 cholesterol transport on cerebral metabolic rate. An understanding of the connection between brain metabolism and brain fat/cholesterol transport may unlock new prevention strategies for treating patients with a comorbidity of metabolic syndrome (MetS) with cognitive impairment. Recent findings suggest that the APOE ε4 carrier impedes the shuttling of lipids from neurons and circumvents the storage of fat within the glia lipid droplets. This sluggish transport of lipids to triglyceride droplets in the glia cells can lead to dangerous reactive oxygen species and hydroxyl-free radicals as lipids are prematurely oxidized.This case study evaluates the effects of a 10-week clinically prescribed ketogenic diet (KD) with a 68-year-old male, heterozygous APOE ε4 carrier, with a dual diagnosis of mild AD and type 2 diabetes (T2DM). The patient was administering both long- and short-acting injectable insulin to mediate his T2DM for 15+ years. Clinical goals of the intervention included increased hypothalamic and peripheral insulin sensitivity as measured via blood ketones with the Abbott Precision Xtra Blood Ketone Meter to confirm metabolic flexibility; controlled plasma glucose as measured via Abbott Precision Xtra Blood Glucose Meter and HgA1c via venous draw; normalization of lipid panel via venous draw and improved memory with restoration of cognitive functionality measured via the Montreal Cognitive Assessment. The Montreal Cognitive Assessment is considered to be a gold standard assessment in the diagnosis of early AD. Physiological biomarkers for T2DM/MetS and cognitive functionality were assessed before/during/after intervention. These measures included HOMA-IR, triglycerides/HDL ratio, HgA1c, fasting glucose, fasting insulin, complete fasting lipid panel and the PEAK mobile application for real-time measurement of cognitive improvement. The results were statistically significant. The patient's baseline Montreal Cognitive Assessment improved from 23/30 (mild AD) to 29/30 (normal ≥ 26). His T2DM was reversed. Pre-intervention HgA1c was 7.8% (T2DM); post intervention HgA1c measured 5.5% (normal). Likewise, the patient achieved statistically significant improvements in the other aforementioned biomarkers of MetS. The results of this case study suggest that a clinically prescribed ketogenic diet has strong potential to restore systemic insulin sensitivity and metabolic flexibility in diabetic, APOE ε4 heterozygous carriers. Mechanisms of action point to normalization of homeostatic negative feedback loops resetting/restoring lipid synthesis/utilization and glucose (insulin)/fatty acid (glucagon) utilization/production in both the body and brain, resulting in increased cerebral metabolism, improved cognition, and reversal of T2DM via renewed cellular insulin sensitivity.

Pilot-Testing of "Healthy Body Healthy Mind": An Integrative Lifestyle Program for Patients With a Mental Illness and Co-morbid Metabolic Syndrome.

Background: Metabolic syndrome and co-morbid physical health conditions are highly prevalent in people with a mental illness. Modifiable lifestyle factors have been targeted to improve health outcomes. Healthy Body Healthy Mind (HBHM) program was developed to provide an integrated evidence-based program incorporating practical diet and exercise instruction; alongside meditation and mindfulness strategies, and comprehensive psychoeducation, to improve the physical and mental health of those with a mental illness.Methods: We report on two data points: (1) Qualitative data derived from the first HBHM program (version 1) exploring its utility and acceptance according to patient feedback; (2) Biometric and mental health data collected on the modified and enhanced 12-week HBHM program (version 2) involving a pilot of 10 participants. Mental and physical health outcomes, weight, abdominal circumference, fasting glucose, cholesterol, and triglycerides were measured at program entry and completion.Results: Qualitative data from HBHM version 1 provided valuable feedback to redevelop and enhance the program. At the end of the HBHM (version 2) 12-week program, a significant mean weight loss of 2 kg was achieved, p = 0.023. There was also a significant reduction in abdominal circumference (mean = 2.55 cm) and a decrease in BMI of almost one point (mean = 0.96 kg/m2), p = 0.046 and p = 0.019, respectively. There were no significant changes in mental health measures or on any other biometrics.Conclusion: Pilot data from the HBHM program found significant reductions in weight and abdominal obesity. The HBHM program could benefit from further modifications, and study replication is required using a controlled design in a larger sample.

Probiotics: A Potential Immunotherapeutic Approach for the Treatment of Schizophrenia.

Probiotics are in use for physiological boosting, health supplement, and for treatment since historical time. Recently, the to-and-fro pathways linking the gut with the brain, explaining the indirect communication via modulation of immune function and levels of various neurotransmitters, have been discovered, but how precisely these modulations alter the levels of neurotransmitters contributing to the cognitive and other symptom improvements in patients with schizophrenia remains a new arena of research for psychiatry and psychology professionals. The germ-free mice experiments have been the game changer in the mechanistic exploration. The antimicrobial usage alters the local gut flora and hence is associated with psychiatric side effects that strengthen the association further. The changes in the genetics of these bacteria with different types of diet and its correlation with neurotransmitters production capacity and the psyche of the individual are indeed an emerging field for schizophrenia research. Redressal of issues such as manufacturing, the shelf life of probiotics, and stability of probiotics in the gut milieu, in the presence of food, secretions, and exact volume needed for particular age group will help in refining the dose duration of probiotic therapy. Clinical trials are underway for evaluating safety and efficacy in schizophrenia. The gut microorganism transplant and pharmacovigilance of probiotics are important areas yet to be addressed accurately. This paper elucidates the pathways, clinical studies, availability of probiotics in the Indian market with their composition, regulatory issues in India about the probiotic use, and future of probiotic research in schizophrenia.

Efektyvnist L-arhininu ta L-karnitynu v skladi kompleksnoho likuvannia khvorykh na hostryi infarkt miokarda z komorbidnym metabolichnym syndromom

Efektyvnist L-arhininu ta L-karnitynu v skladi kompleksnoho likuvannia khvorykh na hostryi infarkt miokarda z komorbidnym metabolichnym syndromom