Lipid metabolism disorder in diabetic kidney disease.

Diabetic kidney disease (DKD), a significant complication associated with diabetes mellitus, presents limited treatment options. The progression of DKD is marked by substantial lipid disturbances, including alterations in triglycerides, cholesterol, sphingolipids, phospholipids, lipid droplets, and bile acids (BAs). Altered lipid metabolism serves as a crucial pathogenic mechanism in DKD, potentially intertwined with cellular ferroptosis, lipophagy, lipid metabolism reprogramming, and immune modulation of gut microbiota (thus impacting the liver-kidney axis). The elucidation of these mechanisms opens new potential therapeutic pathways for DKD management. This research explores the link between lipid metabolism disruptions and DKD onset.

Combined exposure to deoxynivalenol facilitates lipid metabolism disorder in high-fat-diet-induced obesity mice.

Deoxynivalenol (DON) is a trichothecene toxin that mainly produced by strains of Fusarium spp. DON contamination is widely distributed and is a global food safety threat. Existing studies have expounded its harmful effects on growth inhibition, endocrine disruption, immune function impairment, and reproductive toxicity. In energy metabolism, DON suppresses appetite, reduces body weight, triggers lipid oxidation, and negatively affects cholesterol and fatty acid homeostasis. In this study, high-fat diet (HFD) induced obese C57BL/6J mice were orally treated with 0.1 mg/kg bw/d and 1.0 mg/kg bw/d DON for 4 weeks. The lipid metabolism of mice and the molecular mechanisms were explored. The data showed that although DON reduced body weight and fat mass in HFD mice, it significantly increased their serum triglyceride concentrations, disturbance of serum lipid metabolites, impaired glucose, and resulted in insulin intolerance in mice. In addition, the transcriptional and expression changes of lipid metabolism genes in the liver and epididymis (EP) adipose indicate that the DON-mediated increase in serum triglycerides is caused by lipoprotein lipase (LPL) inhibition in EP adipose. Furthermore, DON down-regulates the expression of LPL through the PPARγ signaling pathway in EP adipose. These results are further confirmed by the serum lipidomics analysis. In conclusion, DON acts on the PPARγ pathway of white adipose to inhibit the expression of LPL, mediate the increase of serum triglyceride in obese mice, disturb the homeostasis of lipid metabolism, and increase the risk of cardiovascular disease. This study reveals the interference mechanism of DON on lipid metabolism in obese mice and provides a theoretical basis for its toxic effect in obese individuals.

The Potential Effects of Isoleucine Restricted Diet on Cognitive Impairment in High-Fat-Induced Obese Mice via Gut Microbiota-Brain Axis.

SCOPE: Obesity induced by high-fat diet (HFD) can cause lipid metabolism disorders and cognitive impairment. Isoleucine restriction can effectively alleviate lipid metabolism disorders caused by HFD but the underlying mechanisms on cognition are unknown. METHODS AND RESULTS: Thirty 3-month-old C57BL/6J mice are divided equally into the following groups: the control group, HFD group, and HFD Low Ile group (67% reduction in isoleucine in high fat feeds). Feeding for 11 weeks with behavioral testing, which shows that isoleucine restriction attenuates HFD-induced cognitive dysfunction. As observed by staining, isoleucine restriction inhibits HFD-induced neuronal damage and microglia activation. Furthermore, isoleucine restriction significantly increases the relative abundance of gut microbiota, decreases the proportion of Proteobacteria, and reduces the levels of lipopolysaccharide (LPS) in serum and brain. Isoleucine restriction reduces protein expression of TLR4/MyD88/NF-κB signaling pathway and inhibits upregulation of proinflammatory cytokine genes and protein expression in mice brain. In addition, isoleucine restriction significantly improves insulin resistance in the brain as well as synaptic plasticity impairment. CONCLUSION: Isoleucine restriction may be a potential intervention to reduce HFD-induced cognitive impairment by altering gut microbiota, reducing neuroinflammation, insulin resistance, and improving synaptic plasticity in mice brain.

Protective effects of genistein on the production performance and lipid metabolism disorders in laying hens with fatty liver hemorrhagic syndrome by activation of the GPER-AMPK signaling pathways.

The aim of this study was to evaluate the beneficial effects and potential mechanisms of genistein (GEN) on production performance impairments and lipid metabolism disorders in laying hens fed a high-energy and low-protein (HELP) diet. A total of 120 Hy-line Brown laying hens were fed with the standard diet and HELP diet supplemented with 0, 50, 100, and 200 mg/kg GEN for 80 d. The results showed that the declines in laying rate (P < 0.01), average egg weight (P < 0.01), and egg yield (P < 0.01), and the increase of the ratio of feed to egg (P < 0.01) induced by HELP diet were markedly improved by 100 and 200 mg/kg of GEN treatment in laying hens (P < 0.05). Moreover, the hepatic steatosis and increases of lipid contents (P < 0.01) in serum and liver caused by HELP diet were significantly alleviated by treatment with 100 and 200 mg/kg of GEN in laying hens (P < 0.05). The liver index and abdominal fat index of laying hens in the HELP group were higher than subjects in the control group (P < 0.01), which were evidently attenuated by dietary 50 to 200 mg/kg of GEN supplementation (P < 0.05). Dietary 100 and 200 mg/kg of GEN supplementation significantly reduced the upregulations of genes related to fatty acid transport and synthesis (P < 0.01) but enhanced the downregulations of genes associated with fatty acid oxidation (P < 0.01) caused by HELP in the liver of laying hens (P < 0.05). Importantly, 100 and 200 mg/kg of GEN supplementation markedly increased G protein-coupled estrogen receptor (GPER) mRNA and protein expression levels and activated the AMP-activated protein kinase (AMPK) signaling pathway in the liver of laying hens fed a HELP diet (P < 0.05). These data indicated that the protective effects of GEN against the decline of production performance and lipid metabolism disorders caused by HELP diet in laying hens may be related to the activation of the GPER-AMPK signaling pathways. These data not only provide compelling evidence for the protective effect of GEN against fatty liver hemorrhagic syndrome in laying hens but also provide the theoretical basis for GEN as an additive to alleviate metabolic disorders in poultry.

Fatty liver hemorrhagic syndrome (FLHS) is a nutritional and metabolic disease that seriously threatens the health and performance of laying hens, which is characterized by hepatic steatosis and lipid metabolism disorders. As an isoflavone phytoestrogen, genistein (GEN) exerts many beneficial functions, including alleviating lipid metabolism disorders and anti-inflammatory properties. However, further research is needed on the protective effect and potential mechanism of GEN on the FLHS in laying hens. Here, we found that GEN treatment improved liver injury and decline of production performance in laying hens with FLHS. Moreover, GEN treatment alleviated hepatic steatosis and lipid metabolism disorders through reducing the expression levels of mRNA related to fatty acid transport and synthesis and enhancing the mRNA expression levels of factors associated with fatty acid oxidation in FLHS layers, which may be achieved by activation of the G protein-coupled estrogen receptor­adenosine 5'-monophosphate (AMP)-activated protein kinase signaling pathways. These data not only provide compelling evidence for the protective effects and mechanisms of GEN against FLHS in laying hens but also provide the theoretical basis for GEN to alleviate other metabolic disorders in poultry.

Prevotella intermedia Aggravates Subclinical Hypothyroidism.

Subclinical hypothyroidism (SCH) has been shown to be associated with microbiota. However, the association between SCH and oral microbiota has not yet been elucidated. The results of our previous clinical studies showed that Prevotella intermedia was abundant in the oral microbiota of SCH patients. This study aimed to investigate the relationship between SCH and oral microbiota, verify the pathogenicity of P. intermedia in SCH, and preliminarily explore the possible mechanism. The SCH mouse model with oral application of P. intermedia was established, and the variance in the mouse oral microbiota and changes in thyroid function and metabolism were detected in mice. Student's t test and analysis of variance were used for statistical analysis. Oral application of P. intermedia changed the composition of the oral microbiota of SCH mice, which enhanced the damage to the thyroid and decreased the expression of functional genes of the thyroid. Moreover, P. intermedia decreased oxygen consumption and aggravated glucose and lipid metabolism disorders in SCH mice. Glucose tolerance and insulin tolerance decreased, and the triglyceride content of the liver and inflammatory infiltration in adipose tissue increased in SCH mice after P. intermedia stimulation. Mechanistically, P. intermedia increased the proportion of CD4+ T cells in cervical lymph nodes and thyroids in SCH mice. Th1 cells were suggested to play an important role in the pathogenesis of SCH involving P. intermedia. In conclusion, P. intermedia aggravated SCH manifestations, including thyroid dysfunction and glucose and lipid metabolism disorders, by causing immune imbalance in mice. This study sheds new light on the pathogenesis of SCH from the perspective of oral microbiota.

Consensus document for lipid profile determination and reporting in Spanish clinical laboratories. What parameters should be included in a basic lipid profile? / Documento de consenso para la determinación e informe del perfil lipídico en laboratorios clínicos españoles: ¿Qué parámetros debe incluir un perfil lipídico básico?

Cardiovascular diseases (CVD) continue to be the main cause of death in our country. Adequate control of lipid metabolism disorders is a key challenge in cardiovascular prevention that is far from being achieved in real clinical practice. There is a great heterogeneity in the reports of lipid metabolism from Spanish clinical laboratories, which may contribute to its poor control. For this reason, a working group of the main scientific societies involved in the care of patients at vascular risk, has prepared this document with a consensus proposal on the determination of the basic lipid profile in cardiovascular prevention, recommendations for its realization and unification of criteria to incorporate the lipid control goals appropriate to the vascular risk of the patients in the laboratory reports.

Increased Incidence of Pancreatic Steatosis Detected Using Computed Tomography at Initial Diagnosis of Coronavirus Disease 2019.

BACKGROUND: It is known that hepatic steatosis, diabetes, obesity, and metabolic syndrome are poor prognostic criteria for coronavirus disease 2019. Closely associated with these factors, pancreatic steatosis has yet to be clarified regarding its incidence in patients with coronavirus disease 2019 and its effect on prognosis. This study aimed to compare the incidence of pancreatic steatosis detected in non-contrast chest computed tomography examinations of patients with coronavirus disease 2019 pneumonia at the time of diagnosis with that of the general population. METHODS: In the present retrospective study, which included 399 patients, densities of 5 different regions of the pancreas and 4 different regions of the spleen were measured, and the mean value of the measured densities was obtained. The difference between the mean pancreatic attenuation and splenic attenuation was defined as pancreatic steatosis if pancreatic attenuation-splenic attenuation ≤-5. RESULTS: The median pancreatic density in patients with coronavirus disease 2019 was significantly lower than in those who tested negative (P = .034). In patients who were coronavirus disease 2019 positive, the incidence of pancreatic steatosis was statistically significantly higher (54.3% vs. 43.0%, P = .031). CONCLUSIONS: According to the non-contrast chest computed tomography examination of the patients with coronavirus disease 2019 performed at the time of admission, the incidence of pancreatic steatosis was higher than that of the normal population of a similar age group. Given that patients with pancreatic steatosis and the accompanying metabolic syndrome are more prone to inflammation, the findings suggest that these patients underwent more chest computed tomography examinations at the time of diagnosis. Therefore, pancreatic steatosis may be a poor prognostic factor in coronavirus disease 2019.

The toxicity of nano polyethylene terephthalate to mice: Intestinal obstruction, growth retardant, gut microbiota dysbiosis and lipid metabolism disorders.

Polyethylene terephthalate (PET) are widely used in our daily life while they may be broken to smaller fractions as nano-sized PET (nPET) in the environment. The toxicity of nPET is still less studied. This work first evaluated the LD50 of different size of nPET (200 nm, S-nPET; 700 nm, B-nPET) in mice, then studied the health effects of single exposure to S/B-nPET at 200 mg/kg bw for 30 days. It was found that the LD50 was 266 mg/kg bw for S-nPET and 523 mg/kg bw for B-nPET, respectively, showing a size-dependent effect. S-nPET caused weight loss, cyst, intestinal obstruction, organ damage and mortality (40%), and perturbed gut microbiome and metabolome especially lipid metabolism, such as upregulated cholesterol, glycocholic, propionic acid, niacinamide, ectoine and xanthine, and downregulated arachidonic acid, anserine, histamine, while B-nPET did not. Serological analysis found S-nPET brought more lipid metabolic immune and neurological damage than B-nPET, confirming the size-dependent effect. To the best of our knowledge, this is the first report on the systematic toxicity of nPET to mice. Further studies are warranted for life-long effects of nPET. The protocol applied in this work may also be used for the study of the health effects of other plastics.

[Disorders of lipid metabolism as a risk factor for male infertility].

The presented literature review analyzes and summarizes data on studies by domestic and foreign authors on one of the most pressing problems of modern andrology - the pathogenetic relationship of excess body weight and male infertility. Modern clinical, epidemiological and experimental data indicate a negative effect of obesity on the reproductive function of men. According to the WHO, in Russia 54% of men are overweight, 15% of whom are obese. The problem of obesity is independent of age, area of residence, as well as the social and professional level of men. Obesity is a predisposing factor in the development of concomitant somatic pathological processes. Oxidative stress of sperm, androgen deficiency, neuropathy is far from an exhaustive list of the most important mechanisms for the realization of the neuroendocrine and reproductive effects of overweight and obesity. The increasing number of infertile couples annually dictates the need for a reliable monitoring system to get a correct picture of the development of the obesity epidemic, as well as to quickly assess what preventive measures should be taken.

Farnesoid X Receptor Deficiency Induces Hepatic Lipid and Glucose Metabolism Disorder via Regulation of Pyruvate Dehydrogenase Kinase 4.

Farnesoid X receptors (FXR) are bile acid receptors that play roles in lipid, glucose, and energy homeostasis. Synthetic FXR-specific agonists have been developed for treating nonalcoholic fatty liver disease (NAFLD) patients. However, the detailed mechanism remains unclear. To investigate the effects of FXR on NAFLD and the possible mechanism, FXR-null mice were fed either a normal or a high-fat diet. The FXR-null mice developed hepatomegaly, steatosis, accumulation of lipid droplets in liver cells, glucose metabolism disorder, and elevated serum lipid levels. Transcriptomic results showed increased expression of key lipid synthesis and glucose metabolism-related proteins. We focused on pyruvate dehydrogenase kinase 4 (PDK4), a key enzyme involved in the regulation of glucose and fatty acid (FA) metabolism and homeostasis. Subsequently, we confirmed an increase in PDK4 expression in FXR knockout cells. Moreover, inhibition of PDK4 expression alleviated lipid accumulation in hepatocytes caused by FXR deficiency in vivo and in vitro. Our results identify FXR as a nuclear transcription factor that regulates glucose and lipid metabolism balance through PDK4, providing further insights into the mechanism of FXR agonists in the treatment of metabolic diseases.

Obesity and lipid metabolism disorders determine the risk for development of long COVID syndrome: a cross-sectional study from 50,402 COVID-19 patients.

PURPOSE: Metabolic disorders have been identified as major risk factors for severe acute courses of COVID-19. With decreasing numbers of infections in many countries, the long COVID syndrome (LCS) represents the next major challenge in pandemic management, warranting the precise definition of risk factors for LCS development. METHODS: We identified 50,402 COVID-19 patients in the Disease Analyzer database (IQVIA) featuring data from 1056 general practices in Germany. Multivariate logistic regression analysis was used to identify risk factors for the development of LCS. RESULTS: Of the 50,402 COVID-19 patients included into this analysis, 1,708 (3.4%) were diagnosed with LCS. In a multivariate regression analysis, we identified lipid metabolism disorders (OR 1.46, 95% CI 1.28-1.65, p < 0.001) and obesity (OR 1.25, 95% CI 1.08-1.44, p = 0.003) as strong risk factors for the development of LCS. Besides these metabolic factors, patients' age between 46 and 60 years (compared to age ≤ 30, (OR 1.81 95% CI 1.54-2.13, p < 0.001), female sex (OR 1.33, 95% CI 1.20-1.47, p < 0.001) as well as pre-existing asthma (OR 1.67, 95% CI 1.39-2.00, p < 0.001) and depression (OR 1.27, 95% CI 1.09-1.47, p = < 0.002) in women, and cancer (OR 1.4, 95% CI 1.09-1.95, p = < 0.012) in men were associated with an increased likelihood of developing LCS. CONCLUSION: Lipid metabolism disorders and obesity represent age-independent risk factors for the development of LCS, suggesting that metabolic alterations determine the risk for unfavorable disease courses along all phases of COVID-19.

Carotid sheath xanthoma: A rare manifestation of lipid disorders.

Xanthomas are visibly deformed cholesterol deposits that are commonly associated with lipid disorders, such as familial hypercholesterolemia (FH) or rare sitosterolemia. We present the first report of two cases of carotid sheath xanthomas in patients with lipid disorders. Case 1 involved a 26-year-old woman presenting with two heterogeneous mutations on the ABCG5 gene-as noted on genetic testing-who was finally diagnosed with sitosterolemia. Ultrasonography (US) revealed hypoechoic masses centered in the bilateral carotid sheath, which gradually reduced in size after diet control and the use of ezetimibe. Case 2 involved a 27-year-old man who was diagnosed with possible FH and had recurrent bilateral buttock xanthomas, as well as bilateral carotid sheath masses detected by US. Postoperative pathological examination of the resected right neck mass confirmed a xanthoma with proliferation of multinucleated giant cells and deposition of cholesterol clefts.

Maternal and neonatal outcomes in women with disorders of lipid metabolism.

OBJECTIVES: The effects of lipid metabolism disorders (LMD) on pregnancy outcomes is not well known. The purpose of this study is to evaluate the impact of LMD on maternal and fetal outcomes. METHODS: Using the Healthcare Cost and Utilization Project - National Inpatient Sample from the United States, we carried out a retrospective cohort study of all births between 1999 and 2015 to determine the risks of complications in pregnant women known to have LMDs. All pregnant patients diagnosed with LMDs between 1999 and 2015 were identified using the International Classification of Disease-9 coding, which included all patients with pure hypercholesterolemia, pure hyperglyceridemia, mixed hyperlipidemia, hyperchylomicronemia, and other lipid metabolism disorders. Adjusted effects of LMDs on maternal and newborn outcomes were estimated using unconditional logistic regression analysis. RESULTS: A total of 13,792,544 births were included, 9,666 of which had an underlying diagnosis of LMDs for an overall prevalence of 7.0 per 10,000 births. Women with LMDs were more likely to have pregnancies complicated by diabetes, hypertension, and premature births, and to experience myocardial infarctions, venous thromboembolisms, postpartum hemorrhage, and maternal death. Their infants were at increased risk of congenital anomalies, fetal growth restriction, and fetal demise. CONCLUSIONS: Women with LMDs are at significantly higher risk of adverse maternal and newborn outcomes. Prenatal counselling should take into consideration these risks and antenatal care in specialized centres should be considered.

Molecular Mechanisms of Lipid Metabolism Disorders in Infectious Exacerbations of Chronic Obstructive Pulmonary Disease.

Exacerbations largely determine the character of the progression and prognosis of chronic obstructive pulmonary disease (COPD). Exacerbations are connected with changes in the microbiological landscape in the bronchi due to a violation of their immune homeostasis. Many metabolic and immune processes involved in COPD progression are associated with bacterial colonization of the bronchi. The objective of this review is the analysis of the molecular mechanisms of lipid metabolism and immune response disorders in the lungs in COPD exacerbations. The complex role of lipid metabolism disorders in the pathogenesis of some infections is only beginning to be understood, however, there are already fewer and fewer doubts even now about its significance both in the pathogenesis of infectious exacerbations of COPD and in general in the progression of the disease. It is shown that the lipid rafts of the plasma membranes of cells are involved in many processes related to the detection of pathogens, signal transduction, the penetration of pathogens into the cell. Smoking disrupts the normally proceeded processes of lipid metabolism in the lungs, which is a part of the COPD pathogenesis.

A cohort study on risk factors of high-density lipoprotein cholesterol hypolipidemia among urban Chinese adults.

BACKGROUND: High-density lipoprotein cholesterol (HDL-C) hypolipidemia, a major type of dyslipidemia, has been associated with many kinds of diseases, such as stroke, coronary heart disease, obesity and diabetes, and has displayed an increasing prevalence in China. This study explores the risk factors of HDL-C hypolipidemia and makes recommendations for controlling and preventing HDL-C hypolipidemia and the diseases caused by it. METHODS: Using a retrospective cohort study design, 26,863 urban adults without dyslipidemia, diabetes, cardiovascular and cerebrovascular diseases, hepatosis, renal insufficiency and thyroid diseases were enrolled in the study between 2010 and 2015. Data on each individual were collected at the 2010 baseline year and at a follow-up medical check. A Cox regression model was constructed to evaluate the influence of potential risk factors on the outcome event- HDL-C hypolipidemia. RESULTS: The incidence of HDL-C hypolipidemia was 5.7% (1531/26863). Sex, age, body mass index (BMI), HDL-C, triglyceride (TG) and urea nitrogen (UN) were significant risk factors of HDL-C hypolipidemia. Men were more likely to develop HDL-C hypolipidemia than women during follow-up medical checks (HR = 1.258, P = 0.014). The incidence of HDL-C hypolipidemia in the over 65 years old group was higher than that of the ≤65 age group (HR = 1.276, P = 0.009). The incidence of HDL-C hypolipidemia increased with increasing BMI (HR = 1.030, P = 0.002), TG (HR = 1.321, P = 0.001) and UN (HR = 1.054, P = 0.019), while falling with increasing HDL-C in the baseline year (HR = 0.002, P < 0.001). CONCLUSIONS: Men, aged over 65, with high BMI were at the highest risk of developing HDL-C hypolipidemia. Measures should be taken to prevent HDL-C hypolipidemia even for healthy urban adults whose blood biochemical indicators were in the normal range when their level of TG, UN and HDL-C are closed to the border of the normal value range.

Correction of Lipid Metabolism Disorders in Diabetes Mellitus with Peptide Drugs.

We studied the effect of peptide drugs deltalicin and Semax on lipid metabolism disturbances in diabetes mellitus. Diabetes mellitus was modeled by single injection of streptozotocin (45 mg/kg) and rats with blood glucose ≥12 mmol/liter were selected for the further experiments. Deltalicin in a dose 100 µg/kg and Semax in a dose 200 µg/kg as well as sulodexide corrected lipid metabolism disorders: the content of total cholesterol, triglycerides, LDL, index of atherogenicity decreased and HDL concentration increased. Deltalicin produced more potent effect on lipid metabolism in rats with diabetes mellitus than sulodexide and Semax, which manifested in a significant decrease in total cholesterol and LDL concentration and index of atherogenicity.

High-Performance Liquid Chromatography-Mass Spectrometry-Based Lipid Metabolite Profiling of Acromegaly.

CONTEXT: Metabolic disorders, especially dysregulated lipid metabolism, increase the risk of cardiovascular mortality in acromegaly. Previous studies measuring plasma macromolecular lipids have yielded conflicting results. PURPOSE: To explore the plasma lipid metabolite profiles by metabolomics analysis and identify potential metabolites associated with cardiac function in acromegaly. METHODS: Plasma was obtained from 80 newly diagnosed, untreated patients with acromegaly and 80 healthy controls. Echocardiography was performed. Based on the results of an oral glucose tolerance test (OGTT), patients were categorized into 2 groups: normal glucose tolerance (NGT, n = 28) and impaired glucose tolerance or diabetes mellitus (IGT/DM, n = 52). High-performance liquid chromatography-mass spectrometry (HPLC-MS)-based metabolomics analysis was conducted. Data were processed by principal components analysis (PCA), orthogonal partial least square-discriminant analysis (OPLS-DA), and MetaboAnalyst 4.0. Associations between metabolic substances and cardiovascular parameters were also explored. RESULTS: Metabolomics uncovered a distinct metabolic pattern between acromegaly and healthy controls, and perturbed pathways mainly include glycerophospholipid metabolism, sphingolipid metabolism, as well as linoleic acid metabolism. Collective analysis showed that phosphatidylethanolamine (PE) (22:6/16:0) was positively correlated with LV mass, while lysophosphatidylcholine (LysoPC) (16:0) was positively correlated with fractional shortening (FS) and left ventricle ejection fraction (LVEF). CONCLUSION: Patients with acromegaly have distinct lipid metabolite profiling, while PE (22:6/16:0) and LysoPC (16:0) are correlated with cardiac structure and function, which may contribute to the risk of cardiovascular complications.

Clinical and laboratory parameters and morphological characteristics of the endometrium in women with impaired fat metabolism and failed IVF attempts.

Objective: To study clinical and laboratory parameters and morphological characteristics of the endometrium in women with impaired fat metabolism and failed IVF attempts. Materials and methods: Clinical examination, laboratory tests, morphological analysis, and immunohistochemistry of the endometrium were conducted in 76 patients with different BMI, followed up with infertility and failed IVF attempts. Patients were divided into four groups by body mass index (BMI): 1 group - 17 women with overweight, BMI = 25.0 - 29.9 kg/m2; 2 group - 15 women with class I obesity, BMI 30.0-34.9 kg/m2; 3 group - 14 women with class II obesity, BMI 35.0-39.9 kg/m2; and the control group of 30 women with normal weight, BMI 18.5-24.9 kg/m2. Results: Clinical and laboratory analysis revealed menstrual irregularities and hormonal imbalance such as hypoestrogenism. Immunohistochemistry of the endometrium found a significant decrease in the expression of ERα and PR receptors in the glands correlated to increasing BMI. Conclusion: Pregravid preparation of women with increased BMI and failed IVF attempts has to include life-style modification and weight reduction program to restore normal hormonal status and expression of estrogen and progesterone receptors, prevention of excessive proliferative processes in the endometrium, and improving endometrial receptivity.

Nonalcoholic Fatty Pancreas Disease.

Nonalcoholic fatty pancreas disease (NAFPD) describes a phenotype of pancreatic steatosis (PS) that is not caused by alcohol consumption, viral infections, toxins, or congenital metabolic syndromes but is associated with insulin resistance, malnutrition, obesity, metabolic syndrome, or increasing age. NAFPD is a relatively new disease entity, as the clinical significance of fatty infiltration of pancreas has gained attention recently. Clinical consequences of NAFPD remain largely unknown despite clinical associations. This review aims to study similarities and differences between hepatic and PS and explore recent advances in NAFPD.