High-calorie Diet Research Articles

Rice bran oil reduces organ-specific fat deposition, attenuates hyperlipidaemia and abnormal liver function in Long Evans rats with high fat intake

Introduction: High-calorie diets, particularly the quality of dietary fats, are regarded as an independent risk factor for developing obesity, hyperlipidaemia, and liver diseases. The present study examined the impact of rice bran oil (RBO) on organ-specific fat deposition, lipid profile, and liver function enzymes in Long Evans rats. Methods: Long Evans rats (n=24) were fed for six weeks with a controlled high-fat diet (HFD) to induce hyperlipidaemia and abnormal liver function. Rats were then divided into two groups: one group continued feeding on HFD, and the other group was fed with a RBO diet, replacing the fat source. After six weeks of feeding, six rats from each group were sacrificed and required analytical tests were performed. The remaining obese rats (n=12) were divided into continued HFD and RBO diet, and after sacrificing, essential analytical tests were done. Results: RBO feeding to hyperlipidaemic rats for six weeks significantly reduced brown adipose tissue, abdominal adipose tissue, epididymal adipose tissue, and liver fat compared to continuing HFD group (p<0.05). Similarly, serum levels of total cholesterol, triacylglycerides, and low-density lipoprotein cholesterol were all decreased, whereas high-density lipoprotein cholesterol increased in response to RBO compared to HFD (p<0.05). Additionally, rats fed with RBO showed reduced alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase levels when compared with continuing HFD-fed rats (p<0.05). Conclusion: These findings suggest that RBO supports the reduction of fat storage from major fat depots, controls lipid profile, and restores healthy liver functions in rats.

High Fat Diet and High Sucrose Intake Divergently Induce Dysregulation of Glucose Homeostasis through Distinct Gut Microbiota-Derived Bile Acid Metabolism in Mice.

A high calorie diet such as excessive fat and sucrose intake is always accompanied by impaired glucose homeostasis such as T2DM (type 2 diabetes mellitus). However, it remains unclear how fat and sucrose individually affect host glucose metabolism. In this study, mice were fed with high fat diet (HFD) or 30% sucrose in drinking water (HSD) for 24 weeks, and glucose metabolism, gut microbiota composition, as well as bile acid (BA) profile were investigated. In addition, the functional changes of HFD or HSD-induced gut microbiota were further verified by fecal microbiota transplantation (FMT) and ex vivo culture of gut bacteria with BAs. Our results showed that both HFD and HSD caused dysregulated lipid metabolism, while HFD feeding had a more severe effect on impaired glucose homeostasis, accompanied by reduced hyocholic acid (HCA) levels in all studied tissues. Meanwhile, HFD had a more dramatic influence on composition and function of gut microbiota based on α diversity indices, β diversity analysis, as well as the abundance of secondary BA producers than HSD. In addition, the phenotypes of impaired glucose homeostasis and less formation of HCA caused by HFD can be transferred to recipient mice by FMT. Ex vivo culture with gut bacteria and BAs revealed HFD-altered gut bacteria produced less HCA than HSD, which might closely associate with reduced relative abundance of C7 epimerase-coding bacteria g_norank/unclassified_f_Eggerthellaceae and bile salt hydrolase-producing bacteria Lactobacillus and Bifidobacterium in HFD group. Our findings revealed that the divergent effects of different high-calorie diets on glucose metabolism may be due to the gut microbiota-mediated generation and metabolism of BAs, highlighting the importance of dietary management in T2DM.

Carnosine supplementation and retinal oxidative parameters in a high-calorie diet rat model

BackgroundTo assess oxidative effects induced by a high-calorie diet on the retina of Wistar rats and test the antioxidative effects of carnosine supplementation.MethodsWistar rats were randomly divided into the following groups: standard diet (SD), high-calorie diet (HcD), standard diet + carnosine (SD + Car), and high-calorie diet + carnosine (HcD + Car). The body weight, adiposity index, plasma glucose, total lipids, high-density lipoprotein (HDL), low-density lipoprotein (LDL), uric acid, creatinine, and triglycerides of the animals were evaluated. The retinas were analyzed for markers of oxidative stress. Hydrogen peroxide production was assessed by 2',7'-dichlorodihydrofluorescein diacetate (DCF) oxidation. The total glutathione (tGSH), total antioxidant capacity (TAC), protein carbonyl, and sulfhydryl groups of the antioxidant system were analyzed.ResultsTAC levels increased in the retinas of the SD + Car group compared to the SD group (p < 0.05) and in the HcD + Car group compared to the HcD group (p < 0.05). The levels of GSH and the GSSH:GSSG ratio were increased in the HcD + Car group compared to the SD + Car group (p < 0.05). An increase in the retinal carbonyl content was observed in the HcD group compared to the SD group (p < 0.05) and in the HcD + Car group compared to the SD + Car group (p < 0.05). A high-calorie diet (HcD) was also associated with a decrease in retinal sulfhydryl-type levels compared to the SD group (p < 0.05).ConclusionThe results suggest that feeding a high-calorie diet to rats can promote an increase in carbonyl content and a reduction in sulfhydryl groups in their retinas. The administration of carnosine was not effective in attenuating these oxidative markers.Trial registrationAnimal Ethics Committee of Botucatu Medical School - Certificate number 1292/2019.

ITRAQ-based proteomics reveals the mechanism of action of Yinlai decoction in treating pneumonia in mice consuming a high-calorie diet

ObjectiveTo uncover the underlying mechanisms of action of the Yinlai decoction on high-calorie diet-induced pneumonia through proteomics analysis. MethodsBased on the Gene Expression Omnibus (GEO) database, lung tissue samples from normal and high-fat diet (HFD) fed mice in the GSE16377 dataset were selected as test cohorts to identify differentially expressed genes and conduct bioinformatics analyses. In the animal experiments, mice were randomly divided into the control (N), high-calorie diet pneumonia (M), and Yinlai decoction treatment (Y) groups. Mice in the M group received high-calorie feed and a 0.5 mg/mL lipopolysaccharide solution spray for 30 min for 3 d. The mice in the Y group were intragastrically administered 2 mL/10 g Yinlai decoction twice daily for 3 d. Pathological evaluation of the lung tissue was performed. Differentially expressed proteins (DEPs) in the lung tissue were identified using quantitative proteomics and bioinformatics analyses. The drug-target relationships between Yinlai decoction and core DEPs in the lung tissue were verified using AutoDock Vina and Molecular Graphics Laboratory (MGL) Tools. DEPs were verified by western blot. ResultsGEO data mining showed that an HFD altered oxidative phosphorylation in mouse lung tissue. The Yinlai decoction alleviated pathological damage to lung tissue and pneumonia in mice that were fed a high-calorie diet. A total of 47 DEPs were identified between the Y and M groups. Enrichment analysis revealed their association with energy metabolism pathways such as the tricarboxylic acid cycle (TCA) and oxidative phosphorylation. The protein-protein interaction network revealed that Atp5a1, Pdha1, and Sdha were the target proteins mediating the therapeutic effects of Yinlai decoction. Molecular docking results suggested that the mechanism of the therapeutic effect of Yinlai decoction involves the binding of brassinolide, praeruptorin B, chrysoeriol, and other components in Yinlai decoction to Atp5a1. ConclusionThe Yinlai decoction alleviated lung tissue damage and pneumonia in mice that were fed a high-calorie diet by regulating the TCA and oxidative phosphorylation. Our study highlights the importance of a healthy diet for patients with pneumonia and provides a scientific basis for the prevention and treatment of pneumonia through dietary adjustments.

Tryptophan Prevents the Development of Non-Alcoholic Fatty Liver Disease.

The main aim of this research is to study the protective effects of tryptophan on the histomorphological and biochemical abnormalities in the liver caused by a high-calorie diet (HCD), as well as its ability to normalize mitochondrial functions in order to prevent the development of non-alcoholic fatty liver disease (NAFLD). The study was conducted in male Wistar rats aged 3 months at the start of the experiment. Control animals (group I) were fed a standard diet. Group II experimental animals were fed a diet with an excess of fat (45%) and carbohydrates (31%) for 12 weeks. Group III experimental animals also received L-tryptophan at a dose of 80 mg/kg body weight in addition to the HCD. The presence of NAFLD, functional activity, physiological regeneration, and the state of the liver parenchyma and connective tissue were assessed using physiological, morphological, histo-morphometric, biochemical, and biophysical research methods. HCD induced the development of NAFLD, which is characterized by an increase in liver weight, hypertrophy of hepatocytes and an increase in the concentration of lipids, cholesterol and triglycerides in liver tissue. Increased alanine aminotransferase activity in the liver of obese rats also confirm hepatocytes damage. Tryptophan added to the diet lowered the severity of NAFLD by reducing fat accumulation and violations of bioelectric properties, and prevented a decrease in mitochondrial ATP synthesis. The addition of tryptophan can have a potential positive effect on the liver, reducing the severity of structural, biochemical, mitochondrial and bioelectric damage caused by HCD.

Maternal pea fiber supplementation to a high calorie diet in obese pregnancies protects male offspring from metabolic dysfunction in adulthood.

We investigated the influence of maternal yellow-pea fiber supplementation in obese pregnancies on offspring metabolic health in adulthood. Sixty newly-weaned female Sprague-Dawley rats were randomized to either a low-calorie control diet (CON) or high calorie obesogenic diet (HC) for 6-weeks. Obese animals were then fed either the HC diet alone or the HC diet supplemented with yellow-pea fiber (HC + FBR) for an additional 4-weeks prior to breeding and throughout gestation and lactation. On postnatal day (PND) 21, 1 male and 1 female offspring from each dam were weaned onto the CON diet until adulthood (PND 120) for metabolic phenotyping. Adult male, but not female, HC offspring demonstrated increased body weight and feed intake vs CON offspring, however no protection was offered by maternal FBR supplementation. HC male and female adult offspring demonstrated increased serum glucose and insulin resistance (HOMA-IR) compared with CON offspring. Maternal FBR supplementation improved glycemic control in male, but not female offspring. Compared with CON offspring, male offspring from HC dams demonstrated marked dyslipidemia (higher serum cholesterol, increased number of TG-rich lipoproteins, and smaller LDL particles) which was largely normalized in offspring from HC + FBR mothers. Male offspring born to obese mothers (HC) had higher hepatic TG, which tended to be lowered (p = 0.07) by maternal FBR supplementation.Supplementation of a maternal high calorie diet with yellow-pea fiber in prepregnancy and throughout gestation and lactation protects male offspring from metabolic dysfunction in the absence of any change in body weight status in adulthood.

The obesogenic side of Genistein.

Genistein (GN) has been highly recommended for its medicinal properties like anticancer, antidiabetic, antihyperlipidemic, antiviral, and antioxidant activities among others. Recently, scientists realized that Genistein is an endocrine disruptor. It is an obesogen that interferes with the endocrine system causing obesity through many mechanisms like inducing adipocyte differentiation, lipid accumulation, and transformation of some stem cells into adipocytes (bone marrow mesenchymal stem cells for example) in vitro. Animal studies show that GN upregulates genes associated with adipogenesis like CCAAT/enhancer binding protein alpha (Cebpα), CCAAT/enhancer binding protein beta (Cebpβ), and PPARγ. In silico studies reveal a strong binding affinity for estrogen receptors. All these findings were contingent on concentration and tissues. It is beyond dispute that obesity is one of the most frustrating medical conditions under the sun. The pathophysiology of this disease was first attributed to a high-calorie diet and lack of physical activity. However, studies proved that these two factors are not enough to account for obesity in both children and adults. This mini review highlights how Genistein interaction with the peroxisome proliferator-activated receptor gamma protein can cause obesity.

Effects of a high-fat and high-carbohydrate diet on appetite regulation and central AMPK in the hypothalamus of blunt snout bream (Megalobrama amblycephala).

Adenosine monophosphate-activated protein kinase (AMPK) is a sensor of cellular energy changes and controls food intake. This study investigates the effect of a high-calorie diet (high fat diet [HFD], high carbohydrate diet [HCD]and high energy diet [HED]) on appetite and central AMPK in blunt snout bream. In the present study, fish (average initial weight 45.84 ± 0.07 g) were fed the control, HFD, HCDand HED in four replicates for 12 weeks. At the end of the feeding trial, the result showed that body mass index, specific growth rate, feed efficiency ratioand feed intakewere not affected (p > 0.05) by dietary treatment. However, fish fed the HFD obtained a significantly higher (p < 0.05) lipid productive value, lipid gainand lipid intakethan those fed the control diet, but no significant difference was attributed to others. Also, a significantly higher (p < 0.05) energy intake content was found in fish-fed HFD, HCDand HED than those given the control diet. Long-term HFD and HCD feeding significantly increased (p < 0.05) plasma glucose, glycated serum protein, advanced glycation end product, insulinand leptin content levels than the control group. Moreover, a significantly lower (p < 0.05) complex 1, 2and 3 content was found in fish-fed HFD and HCD than in the control, but no differences (p > 0.05) were attributed to those in HED. Fish-fed HED significantly upregulated (p < 0.05) hypothalamic ampα 1 and ampα 2 expression, whereas the opposite trend was observed in the hypothalamic mammalian target of rapamycinthan those in HFD and HCD compared to the control. However, hypothalamic neuropeptide y, peroxisome proliferator-activated receptor α (pparα), acetyl-coa oxidase and carnitine palmitoyltransferase 1 were significantly upregulated (p < 0.05) in the HCD group, while the opposite was seen in cholecystokininexpression compared to those in the control group. Our findings indicated that the central AMPK signal pathway and appetite were modulated according to the diet's energy level to regulate nutritional status and maintain energy homoeostasis in fish.

Is obesity the next step in evolution through brain changes?

Obesity is a disease of complex and multifactorial nature characterized by the interplay of genetic and environmental factors. The prevailing consensus suggests that obesity arises from an imbalance in energy homeostasis, largely driven by excessive consumption of a high-caloric diet and insufficient physical activity. Over time, therapeutic interventions have traditionally focused on addressing this energy imbalance, as well as the medicalization of all types of obesity. However, there is an alarming increase in the prevalence of obesity, reaching pandemic proportions, with significant consequences for the health of a substantial part of the global population, undoubtedly necessitating a change in strategy.Our purpose is to analyze the obesity pandemic from an evolutionary perspective, and review how its social and cultural causes interact with its pathophysiological determinants. Thus, the culture-brain co-evolution hypothesis is proposed as a compelling framework within niche construction theory that acts as an evolutionary driver for brain expansion and physiological changes in the human species. Some cultural innovations as the invention of tools, and the adoption of processed and cooked foods, have enabled greater energy intake and improved nutrient quality for human diets. These behavioral changes results in the expansion and growth of the human brain, while simultaneously reconditioning the digestive apparatus, leading to a shortening in the time dedicated to foraging and food digestion. These adaptations may have been favored by natural selection, promoting the survival and reproductive success of individuals carrying genetic variants conducive to brain growth and to shape our evolutionary trajectory.In the 20th and 21st centuries, the obesogenic environments were placed in our lifestyles, characterized by extreme sedentary behaviors and the spread of highly processed and high-energy diets. These evolutionary mechanisms may inevitably contribute to the emergence of a new niche that, in addition to explaining the obesity pandemic, could ultimately lead to the “normalization” of phenotypes and genomes associated with obesity. This phenomenon represents a predictable outcome that derives from our biological predispositions developed over countless generations. Addressing this global challenge necessitates the creation of non-obesogenic environments that promote healthy lifestyles to reduce the prevalence of obesity. The failure to take action could perpetuate the current evolutionary trajectory toward a human species characterized by obesity-related genotypes and phenotypes.

Taraxacum mongolicum polysaccharide promotes white adipocyte browning by regulating miR-134-3p via Akt/GSK-3β signalling

In recent years, the incidence of obesity has gradually increased due to high calorie diets and lack of exercise. Reducing energy intake or increasing energy expenditure is the most effective way to promote weight loss and reduce lipid levels. Activated beige adipocytes can increase energy consumption in the body, and inducing conversion of white adipocytes to brown can prevent and treat obesity. Taraxacum mongolicum polysaccharide (TMP) is a plant polysaccharide that has been widely used for its anti-tumour and antioxidant properties. However, little is known about the role of TMP in the browning of sheep white adipose tissue. The aim of this study was to explore the potential mechanism of TMP and miR-134-3p in regulating the browning of sheep white adipocytes, as well as the regulatory relationship between TMP and miR-134-3p. Our results showed that TMP had a positive regulatory effect on the proliferation and browning of sheep white adipocytes. In addition, miR-134-3p significantly inhibited browning activity and AKT/GSK-3β signalling. Importantly, we found that TMP function required miR-134-3p mediation in the browning of sheep white adipocytes. Overall, our results suggested that TMP recruited beige adipocytes by regulating AKT/GSK-3β signalling via miR-134-3p.

Macrophage-restricted overexpression of glutaredoxin 1 protects against atherosclerosis by preventing nutrient stress-induced macrophage dysfunction and reprogramming

Background and aimsDeficiency in the thiol transferase glutaredoxin 1 (Grx1) in aging mice promotes, in a sexually dimorphic manner, dysregulation of macrophages and atherogenesis. However, the underlying mechanisms are not known. Here we tested the hypothesis that macrophage-restricted overexpression of Grx1 protects atherosclerosis-prone mice against macrophage reprogramming and dysfunction induced by a high-calorie diet (HCD) and thereby reduces the severity of atherosclerosis. MethodsWe generated lentiviral vectors carrying cluster of differentiation 68 (CD68) promoter-driven enhanced green fluorescent protein (EGFP) or Grx1 constructs and conducted bone marrow (BM) transplantation studies to overexpress Grx1 in a macrophage-specific manner in male and female atherosclerosis-prone LDLR−/− mice, and fed these mice a HCD to induce atherogenesis. Atherosclerotic lesion size was determined in both the aortic root and the aorta. We isolated BM-derived macrophages (BMDM) to assess protein S-glutathionylation levels and loss of mitogen-activated protein kinase phosphatase 1 (MKP-1) activity as measures of HCD-induced thiol oxidative stress. We also conducted gene profiling on these BMDM to determine the impact of Grx1 activity on HCD-induced macrophage reprogramming. ResultsOverexpression of Grx1 protected macrophages against HCD-induced protein S-glutathionylation, reduced monocyte chemotaxis in vivo, limited macrophage recruitment into atherosclerotic lesions, and was sufficient to reduce the severity of atherogenesis in both male and female mice. Gene profiling revealed major sex differences in the transcriptional reprogramming of macrophages induced by HCD feeding, but Grx1 overexpression only partially reversed HCD-induced transcriptional reprogramming of macrophages. ConclusionsMacrophage Grx1 plays a major role in protecting mice atherosclerosis mainly by maintaining the thiol redox state of the macrophage proteome and preventing macrophage dysfunction.

Research progress on the regulation of oxidative stress by phenolics: the role of gut microbiota and Nrf2 signaling pathway.

In recent years, the increase in high-calorie diets and sedentary lifestyles has made obesity a global public health problem. An unbalanced diet promotes the production of proinflammatory cytokines and causes redox imbalance in the body. Phenolics have potent antioxidant activity and cytoprotective ability. They can scavenge free radicals and reactive oxygen species, and enhance the activity of antioxidant enzymes, thus combating the body's oxidative stress. They can also improve the body's inflammatory response, enhance the enzyme activity of lipid metabolism, and reduce the contents of cholesterol and triglyceride. Most phenolics are biotransformed and absorbed into the blood after the action by gut microbiota; these metabolites then undergo phase I and II metabolism and regulate oxidative stress by scavenging free radicals and increasing expression of antioxidant enzymes. Phenolics induce the expression of genes encoding antioxidant enzymes and phase II detoxification enzymes by stimulating Nrf2 to enter the nucleus and bind to the antioxidant response element after uncoupling from Keap1, thereby promoting the production of antioxidant enzymes and phase II detoxification enzymes. The absorption rate of phenolics in the small intestine is extremely low. Most phenolics reach the colon, where they interact with the microbiota and undergo a series of metabolism. Their metabolites will reach the liver via the portal vein and undergo conjugation reactions. Subsequently, the metabolites reach the whole body to exert biological activity by traveling with the systemic circulation. Phenolics can promote the growth of probiotics, reduce the ratio of Firmicutes/Bacteroidetes (F/B), and improve intestinal microecological imbalance. This paper reviews the nutritional value, bioactivity, and antioxidant mechanism of phenolics in the body, aiming to provide a scientific basis for the development and utilization of natural antioxidants and provide a reference for elucidating the mechanism of action of phenolics for regulating oxidative stress in the body. © 2023 Society of Chemical Industry.

Abstract 13997: Identification of Novel Spectral Densities in Arterial Pressure Time Series for Cardiovascular Risk Stratification in Early Prediabetes: Machine Learning Beyond Conventional Frequency Domain Analysis

Introduction: Despite the extensive use of average BP for diagnosis of cardiovascular disease (CVD), research has shown that changes in BP variability can better reflect CV deterioration. As patients with type 2 diabetes present to the clinic with pre-established CVD, there is a pressing need for early identification of aberrant BP fluctuations useful for risk appraisal. Hypothesis: We hypothesized that deep learning models with superior capacity in feature extraction would enable comprehensive characterization of arterial pressure (AP) time-series allowing CV risk stratification in early prediabetes. Methods: We trained a convolutional neural network (CNN, Figure 1A) to classify spectrograms generated using short-term Fourier transforms of beat-to-beat AP signals collected from control vs. prediabetic rats of both sexes fed a high-calorie diet for 12 or 24 weeks, representing young and old rats. Model performance was assessed on different sampling rates for binary and multi-level classifications of sex, age, and diet. Saliency maps were generated by back-propagation of model scores to extract frequency values crucial for classification. Conventional frequency domain analysis was performed on the original AP time-series and the power spectral densities (PSD) were determined for the frequencies identified for each classification task. PSD were compared among sex, age, and diet groups using 3-way ANOVA and principal component analysis. Results: The model successfully classified AP spectrograms according to age, sex, and diet revealing sex- and age-specific CV deteriorative processes in early prediabetes (Figure 1B-E). Saliency maps identified frequencies of 2, 13, 19, and 43 Hz as crucial for DietxAgexSex classification. Comparison of PSDs for these frequencies was not sufficient for CV risk separation (Figure 1F, G). Conclusions: Employing a CNN overcomes the shortcomings associated with CV risk stratification using conventional methods.

The Effect of Moderate Intensity Interval Training (MIIT) on Short-Term Memory Function, the Ratio of Neocortical Neurons and Glial Cells, and the Number of Hippocampal Pyknotic Granule Cells in Rats on a High-Calorie Diet

Consumption of a high-calorie diet correlates with increased metabolic disturbances that lead to various organ disorders, including neurodegenerative disease. Women are more susceptible to metabolic disorders due to a high-calorie diet, so they have higher risk factors for neuroinflammation. This study was conducted to explain the effect of Moderate Intensity Interval Training (MIIT) on short-term memory, neocortex glia neuron ratio, and hippocampal pyknotic granule cells in female Wistar rats (Rattus norvegicus) with a high-calorie diet. The Wistar rats used were two months old. The study was conducted for four weeks, preceded by the acclimatization of experimental animals. MIIT intervention in the form of swimming is done every 5 minutes with a rest period of 2.5 minutes with two repetitions. Measurement of short-term memory using Y-maze instrument. Results: Before treatment, the highest average body weight was in groups C, B, and A (p=0.006). After treatment, the highest average body weight was found in groups B, C, and A (p=0.569). The test results of short-term memory measurement using the alternation indicator showed no significant difference between groups in the pre-alternation test (p=0.481). There was a significant difference between groups for the neuron-glia ratio (p=0.370) and the hippocampus of the pyknosis granule cells (p=0.078). In conclusion, there is a significant difference between groups A, B, and C towards the MIIT intervention.

EPIGALLOCATECHIN-3-GALLATE ALLEVIATES METABOLIC DISORDERS IN RATS SIMULTANEOUSLY EXPOSED TO ROUND-THE-CLOCK LIGHTING AND KEPT ON HIGH-CALORIE CARBOHYDRATE-LIPID DIET

The aim of the study is to investigate the effect of epigallocatechin-3-gallate (EGCG) on the parameters of carbohydrate and lipid metabolism in the blood serum of rats exposed to round-the-clock lighting (RCL) and kept on high-calorie carbohydrate-lipid diet (HCCLD). The experiments were performed on 21 white Wistar rats weighing 210-250 g, divided into 3 groups. Animals in the first group (control) received a standard diet (energy value 2720 kcal/kg) and were exposed to an equally altered light and darkness periods. The rats of the second and third groups were under the constant round-the-clock light exposure and received HCCLD (4477 kcal/kg). In addition to the conditions in the second group, the test animals of the third group were administered EGCG daily through intragastric gavage in a dose of 40 mg/kg. An enzyme-linked immunosorbent assay kit for rat serum was used to assess insulin concentration. The concentration of serum glucose, total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), and triacylglycerols (TAG) was determined by enzymatic methods using photometric equipment. Insulin resistance was assessed by the HOMA-IR (Homeostatic Model Assessment) index. With the administration of EGCG, the concentration of glucose and insulin in the blood serum decreased by 34.7% and 59.1%, respectively, compared to group 2, and the HOMA-IR was 61.5% lower than in the comparison group. The HDL content increased with the administration of EGCG in the experiment and was 91.3% higher compared to the findings in the group 2. Under these circumstances, the concentrations of VLDL and TAG in the blood serum were significantly lower by 37.5 and 37.1% than the respective values in the group 2. It can be suggested that the administration of the bioflavonoid epigallocatechin-3-gallate significantly alleviates metabolic disorders in rats simultaneously exposed to RCL and kept on HCCLD.

The role of fibrinolysis in the development of prediabetes-associated coronary heart disease: a focus on the plasminogen activator inhibitor -1 and its potential use as a predictive marker in diet-induced prediabetes.

Type 2 diabetes mellitus (T2DM) is associated with an increased risk of cardiovascular diseases (CVD). However, the onset of T2DM is preceded by prediabetes, which is associated with sedentary lifestyles and consumption of high-calorie diets. Studies have shown that impaired glucose homeostasis creates an environment for developing T2DM-related complications. Using a high-fat-high-carbohydrate diet-induced prediabetes animal model, this study sought to assess the risk factors of coronary heart disease (CHD) in diet-induced prediabetes and identify biomarkers that can be used for early detection of prediabetes-associated CHD. Male Sprague Dawley rats were randomly grouped into two groups and were kept on different diets for 20 weeks (n = 6 in each group). One group was fed standard rat chow to serve as a non-prediabetes (NPD) control, while the other group consumed a high-fat-high-carbohydrate diet to induce prediabetes (PD). Post induction, the homeostasis model assessment- insulin resistance (HOMA-IR) and glycated haemoglobin (HbA1c) was used to test for insulin resistance. Body weight, mean arterial pressure (MAP), resting heart rate (HR), inflammatory cytokines (C-reactive protein (CRP), tumor necrosis factor (TNF-α), interleukin-6 (IL-6)), lipids (total cholesterol (TC), triglyceride (TG), lipoproteins (HDL, LDL, VLDL)), endothelial function (endothelial nitric oxide (eNOS), endothelin -1 (ET-1)), fibrinolysis (plasminogen activator inhibitor-1 (PAI-1)) were all measured to assess the risk of CHD. All data were expressed as means ± S.E.M. Statistical comparisons were performed with Graph Pad. Instat Software using Student's two-sided t-test. The Pearson correlation coefficient and linear regression were calculated to assess the association. The value of p < 0.05 was considered statistically significant. There was significant insulin resistance accompanied by significantly increased HbA1c and body weight in PD compared to NPD. Simultaneously, there was a significant increase in inflammatory cytokines in PD compared to NPD. This was accompanied by significantly increased TG and VLDL and endothelial dysfunction in PD. The association between HOMA-IR and PAI-1 was insignificantly positive in NPD, whereas a significantly strong positive association was observed in PD. There is a positive correlation between insulin resistance and PAI-1 during prediabetes; therefore, suggesting that prediabetes increases the risk of developing vascular thrombosis. The current therefore study warrants further investigation on PAI-1 and other markers of fibrinolysis for the early detection of thrombosis and risk of CHD in prediabetes.

Development of a breast cancer risk screening tool for women in Indonesia

BackgroundThe existing challenges related to breast cancer (BC) in Indonesia encompass a significant mortality rate and limited awareness in promptly identifying the risk factors associated with the disease. The objective of this research was to create a screening tool for assessing BC risk among women in Indonesia. MethodsThis study employed a case-control design. The study included a total of 985 women in the case group (those diagnosed with BC) and 985 women in the control group (those without BC), matched for age and sex. The data for this study were obtained from medical records, and primary data collection involved the use of a questionnaire. ResultsThe development of a BC risk screening tool in Indonesia included factors such as age at menopause, age at first pregnancy, family history of BC among first and second-degree relatives, oral contraceptive usage, smoking history, overweight, obesity, high-fat and high-calorie diets, and physical activity levels. The cumulative score derived from the predictor variables ranges from 0 (indicating no risk) to 33 (representing the presence of all risk factors). A total score above 8 indicates a high risk of BC, while a score of 8 or below indicates a low risk of BC. The accuracy of the screening tool was 0.806 (P < 0.001), with a sensitivity of 75.33% and a specificity of 73.20%. ConclusionThe newly developed screening tool shows promise in assessing the risk of BC among women in Indonesia, but additional testing is necessary before it can be recommended for widespread use.

Аnticoagulation Effects of Leucine-Containing Glyprolines in Hypercoagulation

The effects of two leucine-containing glyproline peptides Leu-Pro-Gly-Pro and Pro-Gly-Pro-Leu, including leucine from the N- and C-ends of the molecules, on the parameters of platelet (primary) and plasma hemostasis were studied. Peptides were administered intranasally for 5 days at a daily dose of 500 mcg/kg of body weight under conditions of hypercoagulation caused by intravenous administration of tissue thromboplastin to metabolic syndrome rats on high-calorie diet. Both peptides contributed to an increase in all types of fibrinolysis (total, enzymatic and non-enzymatic), anticoagulant activity and a decrease in platelet aggregation in rat blood plasma compared with the control. The maximum anticoagulant effect was established in a peptide containing leucine from the C-terminus.

The Relevance of a Personalized Low-Normal Protein High-Calorie Diet in Nephrectomized Patients for Renal Cell Carcinoma (RCC): Myth or Reality?

The Relevance of a Personalized Low-Normal Protein High-Calorie Diet in Nephrectomized Patients for Renal Cell Carcinoma (RCC): Myth or Reality?

Characterizing the Metabolic Response of the Zebrafish Kidney to a High-Calorie Diet

Characterizing the Metabolic Response of the Zebrafish Kidney to a High-Calorie Diet