Excessive Fat Intake Research Articles

Acute hyperlipidemia has transient effects on large-scale bone regeneration in male mice

Excessive dietary fat intake increases plasma lipid levels and has been associated with reduced bone mineral density (BMD) and increased risk of osteoporotic fracture, especially in older postmenopausal women. The objective of this study was to investigate whether there are sex-related differences in lipid metabolism that could have an impact on large-scale bone regeneration. Because ribs provide a unique exception as the only bones capable of completely regenerating large-scale defects, we used a rib resection mouse model in which human features are recapitulated. After 10 days of exposure to a low-fat diet or high-fat diet (HFD), we performed large-scale rib resection surgeries on male and female mice (6–7 weeks old) with deletion of the low-density lipoprotein (LDL) receptor (Ldlr−/−) and age- and sex-matched wild-type (WT) mice were used as controls. Plasma analysis showed that short-term exposure to HFD significantly increases total cholesterol, LDL cholesterol, and triglycerides levels in Ldlr−/− mice but not in WT, with no differences between males and females. However, under HFD, callus bone volume was significantly reduced exclusively in male Ldlr−/− mice when compared to WT, although these differences were no longer apparent by 21 days after resection. Regardless of diet or genotype, BMD of regenerated ribs did not differ significantly between groups, although male mice typically had lower average BMD values. Together, these results suggest that short-term hyperlipidemia has transient effects on large-scale bone regeneration exclusively in male mice.

Metabolic outcomes in women 6 months and 2 years after preeclampsia versus normotensive pregnancy: A P4 study.

Preeclampsia is associated with an increased risk of long-term cardiometabolic disease; however, little is known regarding metabolic factors in the early postpartum years potentially contributing to these health disparities. This study aimed to compare body composition, serum biochemical parameters, energy balance and diet 6 months and 2 years after normotensive pregnancy versus preeclampsia. This is the longitudinal metabolic sub-study of the Postpartum Physiology, Psychology and Paediatric cohort study. Women were assessed 6 months and 2 years after normotensive pregnancy (n = 118) and preeclampsia (n = 47). Metabolic measures included anthropometry, body composition via bioelectrical impedance analysis, serum biochemical parameters, diet via a food recall diary, and 24-h energy expenditure using SenseWear Armbands. Two years postpartum, women after preeclampsia continued to have significantly higher weight (median 67.1 kg vs. 63.1 kg, p = .04) compared to normotensive pregnancies, in addition to higher LDL cholesterol levels (2.7 ± 0.8 mmol/L vs. 2.4 ± 0.6 mmol/L, p = .03). These women were also more likely to have an elevated HOMA-IR score ≥2.08 (44% vs. 19%, p = .01). For all women in our study, waist-to-hip ratio, percent fat mass and activity-associated energy expenditure improved overtime. However, HDL cholesterol levels deteriorated, and excess saturated fat and sodium intake persisted from 6 months postpartum. Therefore, two years after preeclampsia, women remain at greater metabolic risk than their normotensive counterparts, with greater weight, LDL cholesterol and markers of insulin resistance, potentially contributing to long-term cardiovascular morbidity and requiring early intervention.

Association between Fat Intake, Dietary Fiber Intake, Physical Activity with Triglyceride Levels among Type 2 Diabetes Mellitus Patients at Grogol Health Center, Sukoharjo

Background: Hyperlipidemia is closely associated with dietary intake and physical activity. Excessive dietary fat intake, inadequate dietary fiber, and low physical activity will increase the risk of obesity and lipid profile disorder among type 2 diabetics. Objectives: This study aimed to identify the association between fat intake, dietary fiber intake, and physical activity with triglyceride levels among type 2 diabetics. Methods: A cross-sectional study was conducted using Sequential Random Sampling on 31 patients with type 2 diabetes with dyslipidemia from Grogol Community Health Center, Sukoharjo, in March 2023. The 3x24-hour food recall nonconsecutive days was used to collect data on fat and fiber intake, the International Physical Activity Questionnaire-Short Form (IPAQ-SF) was employed to obtain physical activity data, and the patient's medical record for the last month was utilized to obtain fasting blood sugar and triglyceride levels. The statistical test was carried out using the Spearman Rank correlation test. Results: Around 54.8% of subjects had excessive fat intake (60.90 g/day); 96.8% of subjects had severe deficit fiber intake (9.74 g/day); 51.6% of subjects had low physical activity (894.74 METs/minute/week). A statistically significant association exists between fat intake and level of triglyceride (p=0.005; r=0.493), but there was no significant association between dietary fiber intake and triglyceride levels (p=0.897; r=0.024), and there was no significant association between physical activity and level of triglyceride (p=0.394; r=-0.159). Conclusions: There is a significant association between fat intake and the level of triglyceride. As such, it is necessary to decrease intakes of saturated fat and trans fatty acids; replacing them with unsaturated fatty acids could be beneficial in lowering triglyceride levels.

Abstract Mo069: Phospholamban Acetylation Enhances Cardiomyocyte Calcium Cycling Under Conditions of High-Fat Feeding

Background: Diet-induced obesity (DIO) is an increasing driver of cardiovascular disease and cardiac dysfunction. The breakdown of excessive fat and sugar intake increases the presence of intracellular acetyl-CoA, which promotes the acetylation of available lysines, altering the stability and activity of these proteins. While numerous proteins involved in cardiac health have been identified as targets of acetylation, the impact of acetylation on calcium handling sarcoplasmic reticulum (SR) proteins, particularly the SERCA2a regulator phospholamban, remains poorly understood. Hypothesis: Phospholamban acetylation is upregulated by exposure to high fat conditions, in turn driving SERCA2a activity and promoting faster calcium SR reuptake. Approach: Left ventricle (LV) tissue from DIO mice and controls, and human LV tissue from control and diabetic patients, was collected and analyzed using immunoblotting and acetylation was quantified by immunoprecipitation with acetyl-lysine antibodies.Isolated working hearts from DIO and control mice were assessed before and after treatment with acute HDAC activator ITSA-1 and SIRT1 activator SRT1720 to promote deacetylation. Adult ventricular cardiomyocytes were isolated from DIO and control mice, and DIO cells were incubated in media containing excess lipid substrates (1% Lipid Mix 1, Millipore Sigma) and ITSA-1 orSRT1720. Changes in stimulated calcium dynamics were assessed using Fura-2AM and Fluo-4AM imaging. Acetylmimetic/acetylation incompetent PLN mutants were transfected into cultured cells to evaluate SERCA2a binding, oligomerization, and FRET efficiency. Results: Phospholamban acetylation significantly increased in LV tissue from both DIO mice and human diabetic patients. Acute treatment of isolated hearts and isolated cardiomyocytes from DIO mice with HDAC and SIRT1 activators significantly reduced contractility, relaxation, and SR calcium reuptake rates. Mutations in PLN mimicking or preventing lysine acetylation altered oligomerization and SERCA2a binding. Conclusions: Obesity increases the acetylation of phospholamban and enhances the reuptake of calcium into the SR, while deacetylation reverses these effects. These data directly tie nutritive status to a novel phospholamban post-translational modification that may directly impact myocardial calcium handling and contractile function.

Effect of alcohol consumption on lipid profile

Now-a-days alcoholism is major complication for development of different diseases. According to our literature review chronic alcoholic consumption will cause the lot of health complications. People without any comorbidities are also diagnosed with the lot of health complications at early age because of alcohol consumption. Our aim of the study is to identify the lipid changes in chronic alcoholic patients and how it effects on their health.To monitor the lipid changes in alcoholic persons.A prospective observational study was conducted for duration of six months, the data has been collected in 456 patients over six months of period and the data was collected with informed consent from the persons. All the data was collected by interacting with persons by using data collection form and laboratory reports were studied.In our study, 456 male populations were included. Out of 456 members, 272 people were alcoholics, and 184 members were non-alcoholic. Out of 272 population 180 are chronic alcoholics and 92 are occasional alcoholics. Out of 456 members young adults (18-25) 182 (39.9%) persons and old adults (26-40) were 274 (60%) persons296 members are taking alcohol with food and 160 members are taking without food. Out of 456 population 438 (96%) persons are non-vegetarians and 18(4%) members are vegetarians. Out of 272, 104 members were drinking beer, 58 were cheap liquor, 25 were Officers' choice, 18 were royal stag, 22 were blenders pride, 15 were signature, 23 were mixed brands, and 7 were others. In our study 156 persons were drinking sweetened beverages, 52(33.3%) members are daily beverage intakes and 104(33.3%) Members are occasionally beverage intakes. According to our study most commonly used sugary beverage brands are thumps up 93(59%), 48(31%) Sting,15(10%) other sugary beverages. Out of 156, Triglycerides were elevated in 47 and LDL was elevated in 36 persons, VLDL elevated in 4 persons and T. Cholesterol elevated in 5 members, Normal lipid profile in 64 persons. Out of 456 persons, 314(69%) are undiagnosed and 142(31%) are diagnosed with lipid changes. According to our common complications associated with alcohol consumption 39 were cardiac, 56 were hepatic, 9 were renal, and 38 were others (pancreatitis, stroke, cholelithiasis).In our study, we concluded that alcohol consumption will mainly affect triglyceride levels. Elevation of triglyceride levels is associated with the quantity and duration of alcohol intake. Normal Intake of alcohol does not cause lipid changes. Excessive intake of beer and cheap liquor increases TG. Excessive alcohol intake and fat intake will increase the LDL, Triglycerides, VLDL and decrease HDL. Excessive intake of sweetened beverages may also cause dyslipidaemia. Because it contains a high number of calories. The most common complication associated with elevation of triglycerides are hypertension, cardiovascular disease. Alcohol intake with food or without food shows the same complications but the absorption of alcohol may vary with food. Alcohol consumption with fat intake will cause hyperlipidaemia.

The Recombinant Lactobacillus Strains with the Surface-Displayed Expression of Amuc_1100 Ameliorate Obesity in High-Fat Diet-Fed Adult Mice.

Excessive dietary fat intake is closely associated with an increased risk of obesity, type 2 diabetes, cardiovascular disease, gastrointestinal diseases, and certain types of cancer. The administration of multi-strain probiotics has shown a significantly beneficial effect on the mitigation of obesity induced by high-fat diets (HFDs). In this study, Amuc_1100, an outer membrane protein of Akkermansia muciniphila, was fused with green fluorescent protein and LPXTG motif anchor protein and displayed on the surface of Lactobacillus rhamnosus (pLR-GAA) and Lactobacillus plantarum (pLP-GAA), respectively. The localization of the fusion protein on the bacterial cell surface was confirmed via fluorescence microscopy and Western blotting. Both recombinant strains demonstrated the capacity to ameliorate hyperglycemia and decrease body weight gain in a dose-dependent manner. Moreover, daily oral supplementation of pLR-GAA or pLP-GAA suppressed the HFD-induced intestinal permeability by regulating the mRNA expressions of tight junction proteins and inflammatory cytokines, thereby reducing gut microbiota-derived lipopolysaccharide concentration in serum and mitigating damage to the gut, liver, and adipose tissue. Compared with Lactobacillus rhamnosus treatment, high-dose pLR-GAA restored the expression level of anti-inflammatory factor interleukin-10 in the intestine. In conclusion, our approach enables the maintenance of intestinal health through the use of recombinant probiotics with surface-displayed functional protein, providing a potential therapeutic strategy for HFD-induced obesity and associated metabolic comorbidities.

Effects of genetic disclosure on SNPs rs1761667, rs8065080, and rs662799 on the limitation of salt and fat intake

Excess salt and fat intake in our food leads to a higher risk of obesity and hypertension. One of the factors that affect our preference is genetics, where a person's preference is related to single nucleotide polymorphisms (SNPs) in taste receptors can also influence food choices. Currently, several prog to limit salt intake are often unsuccessful because lack of individual motivation. Therefore, this study aimed to examine the effect of genetic disclosure on salt limitation and fat intake. The study recruited forty-one adult participants aged 20-50 years who underwent a 14-day healthy transformation Nutricare program organized by PT. Nutrifood Indonesia. Participants were divided into two groups, the first group (n = 20) as the control group and the second group (n = 21) as the genetic disclosure group. The genetic disclosure was performed with rs8065080 on the TRPV1 gene (related to salty taste sensitivity), rs1761667 in the CD36 gene (related to fatty taste sensitivity), and rs662799 in the APOA5 gene (related to the hyperlipidemia risk). Overall, 90% of genetic disclosure group participants showed a significant reduction in salt (7.02±2.25 g/day vs. 4.42±1.98 g/day, p = 0.002) and fat (70.84±18.45 g/day vs 48.54±12.25 g/day, p = 0.000) intake. Results comparison between groups also showed that the group with genetic information resulted in a greater decrease in the intake of salt (-1.95±2.28 vs. 2.60±3.05, p = 0.397) and fat (-11.43±22.01 vs -22.31±21.46, p = 0.1). Therefore, genetic disclosure could help individuals live healthier by motivating the participants to reduce salt and fat intake.

Association of specific nutritional intake with periodontitis

BackgroundThe present study aimed to evaluate nutritional intake among a group of male patients in the dental clinic with and without periodontal disease to search for associations between nutritional profile and periodontal health.MethodsTo this purpose, nutritional intake of macronutrients, fiber, vitamins, and minerals were compared evaluating both clinical parameters and periodontal status. Non periodontitis patients were compared with stage III and IV periodontitis and its extension according to the 2017 classification.ResultsAfter multivariate analysis, statistically significant associations were found between the dietary intake of energy, total fat, cholesterol, calcium, saturated fat, monounsaturated fat and folic acid and iodine and periodontitis status. This study reports an inverse association between cholesterol and iodine and periodontitis and a direct association with saturated fat, monounsaturated fat, and folic acid.ConclusionsMaintaining an adequate intake of fat, iodine, calcium, and cholesterol and avoiding an excessive intake of energy, saturated fat, monounsaturated fat, and folic acid could be important to controlling periodontitis.

Magnoflorine Ameliorates Chronic Kidney Disease in High-Fat and High-Fructose-Fed Mice by Promoting Parkin/PINK1-Dependent Mitophagy to Inhibit NLRP3/Caspase-1-Mediated Pyroptosis.

Excessive intake of fat and fructose in Western diets has been confirmed to induce renal lipotoxicity, thereby driving the progression of chronic kidney disease (CKD). This study was conducted to evaluate the efficacy of magnoflorine in a CKD mouse model subjected to high-fat and high-fructose diets. Our results demonstrated that magnoflorine treatment ameliorated abnormal renal function indices (serum creatinine, urea nitrogen, uric acid, and urine protein) in high-fat- and high-fructose-fed mice. Histologically, renal tubular cell steatosis, lipid deposition, tubular dilatation, and glomerular fibrosis were significantly reduced by the magnoflorine treatment in these mice. Mechanistically, magnoflorine promotes Parkin/PINK1-mediated mitophagy, thereby inhibiting NLRP3/Caspase-1-mediated pyroptosis. Consistent findings were observed in the palmitic acid-incubated HK-2 cell model. Notably, both silencing of Parkin and the use of a mitophagy inhibitor reversed the inhibitory effect of magnoflorine on NLRP3 inflammasome activation in vitro. Therefore, the present study provides compelling evidence that magnoflorine improves renal injury in high-fat- and high-fructose-fed mice by promoting Parkin/PINK1-dependent mitophagy to inhibit NLRP3 inflammasome activation and pyroptosis. Our findings suggest that dietary supplementation with magnoflorine and magnoflorine-rich foods (such as magnolia) might be an effective strategy for the prevention of CKD.

Applying Resistant Starch to Improve the Gel and Water Retention of Reduced-Fat Pork Batter.

Emulsified meat products contain high animal fat content, and excessive intake of animal fat is not good for health, so people are paying more and more attention to reduced-fat meat products. This study investigated the impact of varying proportions of pork back-fat and/or resistant starch on the proximate composition, water and fat retention, texture properties, color, and rheology characteristic of pork batter. The results found that replacing pork back-fat with resistant starch and ice water significantly decreased the total lipid and energy contents of cooked pork batter (p < 0.05) while improving emulsion stability, cooking yield, texture, and rheology properties. Additionally, when the pork back-fat replacement ratio was no more than 50%, there was a significant increase in emulsion stability, cooking yield, hardiness, springiness, cohesiveness, chewiness, and L* and G' values (p < 0.05). Furthermore, resistant starch and ice water enhanced myosin head and tail thermal stability and increased G' value at 80 °C. However, the initial relaxation times significantly decreased (p < 0.05) and the peak ratio of P21 significantly increased from 84.62% to 94.03%, suggesting reduced fluidity of water. In conclusion, it is feasible to use resistant starch and ice water as a substitute for pork back-fat in order to produce reduced-fat pork batter with favorable gel and rheology properties.

Exploring Atherosclerosis, Oxidized LDL, Insulin, and Tailored Diet Strategies in Cardiac Patient Assessment

Background Plaque development in vessels which supply blood to heart muscles is caused by atherosclerosis, a slow but progressive process that leads to coronary artery disease (CAD). Arteries become gradually blocked by oxidized fatty acids, with excess fat intake or abnormalities in fat metabolism causing body changes. These changes may lead to an increase in LDL cholesterol, triglycerides, as well as a reduction in HDL cholesterol. The oxidation of excess low density protein (LDL) is a complex process involving many factors, with insulin and obesity playing a significant role and associated with many metabolic syndromes. The current study aims to determine the concentration of oxidized LDL in patients who suffer with cardio vascular diseases (CVDs) and to understand the correlation between oxidation and insulin resistance in cardiac forbearing. Method The method used was to collect data from 30 patients admitted in the cardiology ward. For this purpose, an assessment proforma was built, which included anthropometric measurements, physical activity level, dietary history, and blood tests for lab findings such as lipid profiles. Results The key findings determined that the anomalous function of AKT protein, which is present in pancreatic β cells, as well as disruption in PKC pathway cause phosphorylation in alpha and beta cells of pancreas, which causes diabetes and leads to heart attack. Conclusion The aberrant changes in sugar test and lipid profile including Hb1Ac (9%), fasting blood glucose (250mg/dl), total cholesterol (342mg/dl), LDL (less than 250mg/dl), HDL (49 F mg/dl), and total triglycerides (215mg/dl) causes serious discomfort for patients.

Metabolic Effects of Short-Term High-Fat Intake Vary Depending on Dietary Amino Acid Composition

BackgroundIt is generally accepted that excessive fat intake has undesirable effects on the energy metabolism of our body. Dietary amino acid composition is also critical to the regulation of lipid metabolism. ObjectivesThis study aimed to investigate whether high-fat diets (HFDs) with different amino acid deficiencies lead to different metabolic outcomes. MethodsSix-wk-old male Wistar rats were fed either a control diet (CN; 3.7 kcal/g, 12% calories from fat) or HFDs (5.1 kcal/g, 60% calories from fat) with 7 different amino acid compositions [control or methionine, arginine, histidine, lysine, threonine, or branched-chain amino acids (BCAAs) deficient], for 7 d. Tissue weights and lipid accumulation in the liver, skeletal muscle, and adipose tissue were measured, and serum biochemical parameters were analyzed. ResultsAlthough the food intake of the HFD groups was a little less than that of the CN group, the total calorie intakes were comparable among the groups, except for histidine-deficient and BCAA-deficient groups. In rats fed am HFD with a control amino acid composition (HFCN), dramatic increase in triglyceride (TG) accumulation in the liver and serum LDL cholesterol concentration were observed compared with the CN group. However, when the arginine content in the diet was reduced, liver TG accumulation was completely inhibited, with no apparent effects on serum lipoprotein-cholesterol concentrations. Meanwhile, deficiency of the other amino acids, such as threonine, reversed HFD-induced upregulation of serum LDL cholesterol. ConclusionsIt is observed that although the rats ingested an excessive amount of fat, neither ectopic fat accumulation nor dyslipidemia were always induced at least in the short term; hence, the consequent metabolic change was dependent on the dietary amino acid composition. These findings introduce an important perspective regarding HFD regimens in both scientific and clinical contexts.

Spatial and temporal evolution of liver cancer incidence

Liver cancer has become a global public health problem and is the fourth leading cause of death and the sixth most common cancer worldwide. The article comprehensively constructed a system of indicators to measure the level of liver cancer incidence from three aspects: economy, diet, and health indicators, and analyzed the influencing factors of liver cancer incidence in 204 countries and regions in the world and the geographical characteristics of the level by using multivariate statistical analyses such as the coefficient of variation method and geodetector. The study shows that (1) the incidence rate of liver cancer is lower in countries with higher GDP levels and urbanized population rates. (2) The combination of caloric intake and protein intake had the largest interaction effect on liver cancer incidence. (3) Excessive fat and protein intake will increase the burden on the liver and cause an increase in the incidence of liver cancer.

Liver PKCε Heterozygous (LivPKCεfl/Δ) Female Mice Showed Better Glucose Tolerance than LivPKCεfl/Δ Male Mice When Fed on High Fat or High Fructose Diet for One Month

Introduction: Excess intake of high fat (HFD) and high fructose (HFrD) diets leads to liver fat accumulation that are linked with insulin resistance, glucose intolerance, hepatosteatosis and diet induced obesity. Activation of liver protein kinase Cε (PKCε) has been implicated as a key mediator of diet induced hepatic insulin resistance. However, this mechanism is not fully understood. Using PKCε knockout (PKCε-KO) mice, we aim to investigate the molecular mechanisms of how PKCε may interact with the insulin signaling cascade in both HFD and HFrD induced insulin resistance and obesity. Hypothesis: Studies have shown that PKCε−/− mice are protected from diet-induced insulin resistance and fasting-state glucose homeostasis was enhanced in PKC-KO mice. We hypothesize that hepatic PKCε deletion will protect against HFD and HFrD induced glucose intolerance in mice. Methods: In order to generate liver specific PKCε−/− mice, we crossed female PKCεfl/fl mice with male Alb Cre+/+ mice. At the time of this study, we have generated heterozygous (PKCεfl/Δ) mice which are being crossed to develop homozygous PKCε knockout (LivPKCεΔ/Δ) mice. Both Male and Female heterozygous (PKCεfl/Δ) mice were placed on three diets: Control (Cntrl, Research Diets Inc, RDI D12450J, Protein (20%), Carbs (70%, corn starch-50%, sucrose-maldextrin-20%, fructose-0%), Fat 10% (lard)), High Fructose (HFrD, RDI D02022704), Protein (20%), Carbs (70%, corn starch-50%, sucrose-maldextrin-20%, fructose-60%), Fat 10% (lard)) and High Fat (HFD, RDI D12492, Protein (20%), Carbs (20%, corn starch-0%, sucrose-maldextrin-20%, fructose-0%), Fat 60% (lard)). Within 1 month on the diets, the mice were genotyped and glucose tolerance tests (GTT, 2 g/kg body weight) were performed following 6 hours of starvation. Results: Our preliminary results showed that within one month, LivPKCεfl/Δ-HFD and LivPKCεfl/Δ-HFrD female mice displayed better glucose tolerance than male mice as seen by their lower glucose level during GTT. Interestingly, both LivPKCεfl/Δ male and LivPKCεfl/Δ female mice did not show significant differences in glucose tolerance when they were on control diet (LivPKCεfl/Δ-Cntrl) within the same duration. Conclusion: Conflicting evidence exists whether liver or adipose tissue specific deletion of PKCε protects mice from diet induced glucose intolerance. Studies in both humans and rodents have demonstrated that female subjects experience less endogenous glucose production and less hepatic insulin resistance than their male counterparts after high fat or high fructose challenge (PMID 23049932, PMID 18332156) and our preliminary findings are in line with these studies. Subsequent studies will use homozygous PKCε (LivPKCεΔ/Δ) mice and their littermates Wild-type mice for in-depth metabolic and molecular analysis. We would like to thank the National Science Foundation for award # NSF1931045 and the National Institutes of Health, award # 1R01DK126892-01A1. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Deletion of SGK1 in Smooth Muscle Cells Induces Sex-specific Differences in Obesity-mediated Metabolic Dysfunction and Adipose Tissue Remodeling

Objectives: Obesity, characterized by an excess of adipose tissue, is an important risk factor for the development of metabolic diseases such as type 2 diabetes. In obesity, poor metabolic health is partly due to glucose intolerance, a condition in which whole-body glucose regulation is impaired. Adipose tissue is an endocrine organ central for optimal metabolic health and its expansion by excessive fat intake induces metabolic dysfunction. The molecular mechanisms that promote metabolic dysfunction in obesity are not fully understood. Adipose tissue function is dependent on the presence of new vascular networks capable of supplying nutrients and oxygen during adipose tissue expansion. Thus, pathological vascular remodeling may promote adipose tissue expansion and dysfunction in obesity. In this regard, our previous studies have shown that serum and glucocorticoid-inducible kinase 1 (SGK1) in vascular smooth muscle cells (vSMCs) mediates pathological vascular remodeling in obesity. SGK1 is a serine/threonine kinase that becomes elevated in the vasculature during obesity and is implicated in the development of metabolic syndrome. Therefore, we hypothesize that smooth muscle cell derived-SGK1 promotes pathological adipose tissue remodeling and metabolic dysfunction during obesity by perturbing adipose tissue vascularization. Methods: To test this hypothesis, these studies utilized our novel SMC-specific SGK1 knockout (smSGK1KO) mouse model to study the influence of SMC-derived SGK1 on adipose tissue remodeling and overall metabolic health in vivo. Male and female 8-week-old smSGK1WT and smSGK1KO mice were subjected to either a 10% low-fat diet (LF) or a high-fat diet (HF) for 8 weeks with weekly body weight measurements. Upon completion of respective diets, mice were subjected to glucose tolerance tests (GTT) to assess glucose tolerance and metabolic health. Adipose tissues from the subcutaneous (inguinal) and intra-abdominal (epididymal/gonadal) white adipose tissue (WAT) depots were harvested to assess overall adiposity and vascularization. Results: Our data show sexual dimorphism exists in the way smSGK1KO mice respond to a chronic high-fat diet. When fed a HF diet, female smSGK1KO mice gained approximately 60% more weight than their female smSGK1WT counterparts. In contrast, weight gain was about 50% lower in male smSGK1KO compared to male smSGK1WT mice on the same HF diet. Despite the differences in weight gain, inguinal and epididymal/gonadal WAT were reduced in male and female smSGK1KO mice fed a HF diet. Surprisingly, GTT was similar between female smSGK1KO and smSGK1WT mice, despite the increased weight gain, while male smSGK1KO mice displayed improvement in glucose tolerance in comparison to their wildtype counterparts. Moreover, male smSGK1KO mice appear to have enhanced vascularization in WAT depots as evidenced by increased vascular branching in fat pads. Conclusions: These studies suggest that SGK1 in smooth muscle cells contributes to adipose tissue remodeling and metabolic dysfunction under obesogenic conditions. Additionally, these studies indicate a need to understand the mechanisms by which crosstalk between the vasculature and adipose tissue modulates obesity and overall metabolic health. This research is supported in part by grant number 5U24DK132733-02 from the National Institute of Health, NIH. This research is supported in part by grant number 5T32HL007609-36 from the National Institute of Health, NIH. This research is supported in part by grant number 2100832 from the National Science Foundation, NSF. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Consumer Preferences and Willingness to Pay for High-Quality Vegetable Oils: A Cross-Sectional Analysis of Chinese Residents.

The consumption of edible vegetable oil is an important source of essential fatty acids and vitamin E for the human body. Guiding residents to consume scientifically and reasonably control the intake of edible oils is an important part of promoting the construction of a healthy China. Currently, Chinese residents have an insufficient understanding of the scientific consumption of edible oils, leading to an intake exceeding the dietary recommendations, resulting in excessive fat intake and increasing the risk of chronic diseases such as obesity and cardiovascular diseases. Based on the Theory of Planned Behavior (TPB) and using Structural Equation Modeling (SEM), this study analyzed the cognitive preferences and willingness to pay a premium for edible vegetable oils among urban consumers in China. The survey included 1098 Chinese urban consumers of vegetable oils. The research found that attitudes, health value, monetary value, and environmental endowment of urban residents are the main predicting factors of the intention to purchase high-quality vegetable oils. This study confirms the applicability of the Theory of Planned Behavior in the consumption of high-quality vegetable oils and provides theoretical contributions and insights for Chinese enterprises and policymakers in formulating marketing strategies for vegetable oils.

Dietary fat consumption frequency and body mass index of middle-age adults in Mumbai city, India during COVID-19 pandemic

Obesity and COVID-19 are global pandemics listed by World Health Organization, which need urgent attention. Obesity involves low grade chronic inflammation, which is characterised by sustained pro-inflammatory innate immune responses mediated through activation of the NLR family pyrin domain-containing 3 (NLRP3) inflammasome/IL-1 axis, and is a strong risk factor for Diabetes and Heart diseases(1). Dietary fats provide energy, satiety, source of fat-soluble vitamins and essential fatty acids – Omega 3 (n-3) and Omega 6 (n-6) fatty acids, but must be consumed in right amounts and ratios. Essential fatty acids (EFA) deficiency and n-6/n-3 imbalance is linked with chronic illnesses such as, heart attacks, cancer, insulin resistance, stroke, obesity, and diabetes(2). Excess dietary fat intake and imbalance of fatty acids, contribute to obesity, inflammation, comorbidities and faster disease progression. A cross-sectional survey aimed to understand the fatty food frequency of overweight and obese middle age adults from Mumbai, India during the COVID-19 outbreak. Using purposive sampling, 100 adults (30-60 years), a questionnaire (demographics, anthropometrics and fat food frequency questionnaire) was administered. Data was analysed using SPSS 26.0. As per BMI standards, 60.2% participants were overweight, 12.6% were obese and 27.1% had normal BMI. For visible fat consumption, sunflower oil (47.6%), ghee (38.8%), rice bran oil (34%) groundnut oil (11.7%) and invisible fats – milk (100%). Other dairy products, nuts and oilseeds were consumed weekly. twice a week, majority (92.3%) consumed packaged high fat foods as compared to eating deep-fried items (58.9%). We concluded that excess dietary fat intake is high risk factor for obesity and related comorbidities diabetes, and hypertension. High BMI increases the risk for non-communicable diseases (NCDs) such as obesity, cardiovascular disease (CVD), insulin resistance and type 2 diabetes. People with co-morbidities are high risk groups for COVID-19 infection susceptibility. Hence, managing weight could be a cost-effective preventive strategy to help in delaying the onset and progression of NCDs, thereby lowering the susceptibility to COVID-19. Our findings have important implications in working towards adopting healthy fats and reducing mortality and reducing the global burden of pandemic. High dietary fat intake is a modifiable risk factor for overweight and obesity. Comorbidities increased risk for COVID-19 infection, disease severity and mortality. Hence, there is a need to understand the dietary fat consumption patterns in obesity and COVID-19. Dietary carbohydrate, sugar and fat quality in relation to obesity and pandemic such as, COVID-19 could be explored in future studies.

Nutrition Assessment and Management in Celiac Disease

Celiac disease (CeD) is the most common immune condition affecting the gastrointestinal tract; it is triggered by gluten and the only available treatment is a strict gluten-free diet (GFD). Therefore, for patients with CeD, adopting a GFD is not a lifestyle choice. The major problem is that a GFD is restrictive and, like all restrictive diets, it has the potential for adverse nutritional outcomes, especially if adopted for a long term. It is well known that GFD can be nutritionally inadequate and is frequently associated with vitamin and mineral deficiencies; it is also associated with excessive sugar and fat intake, particularly when gluten-free substitutes are consumed. Consequently, people with CeD are affected by higher rates of overweight and obesity and metabolic complications, such as fatty liver and cardiovascular disease. Therefore, assessment of nutritional status and diet quality at diagnosis and while on a long-term GFD is key in the management of CeD. This narrative review addresses nutritional considerations in CeD and management of common challenges associated with a GFD.

Gender Disparities in Dietary and Addiction-Associated Risk Factors of Hypertension: Insights from Karachi

Objectives: This study aimed to investigate the dietary and addictive risk factors associated with hypertension and assess their gender-specific patterns. Methodology: Conducted at the Outpatient Department of Medicine, Jinnah Postgraduate Medical Centre, Karachi, from July to December 2022, this descriptive cross-sectional study enrolled diagnosed hypertensive patients with a history of elevated blood pressure lasting more than six months, using a nonpurposive convenient sampling technique. Detailed histories of addictive and dietary risk factors were obtained, and blood pressure was measured. Dietary risk factors included excessive salt and fat intake, along with a diet rich in saturated fatty acids. Addictive risk factors assessed included tobacco and areca nut addiction. Results: Of the 960 patients included, 588 (61.2%) were male, and 372 (38.8%) were female. Males exhibited poorer hypertension control (42.0%) compared to females (33.7%). The most prevalent dietary risk factor was excessive fat intake (76.7%), followed by excessive salt intake (66.7%). Smoking was reported in 66 (11.2%) males and 4 (1.0%) females, while areca nut addiction was observed in 51 (8.5%) males and 15 (4.0%) females. Conclusion: Our findings underscored a significant association between male gender and inadequate hypertension control, coupled with a higher prevalence of dietary and addiction-related risk factors. These findings highlight the importance of targeted interventions aimed at mitigating these modifiable risk factors, particularly among males, to reduce the burden of hypertension-related morbidity and mortality.

Time-dependent impact of a high-fat diet on the intestinal barrier of male mice.

Excessive saturated fat intake compromises the integrity of the intestinal mucosa, leading to low-grade inflammation, impaired mucosal integrity, and increased intestinal permeability, resulting in the migration of lipopolysaccharide (LPS) to other tissues. To evaluate the chronic effects (at 10 and 16 wk) of a high-fat diet (HFD) (with 50% energy as fat) on the phylogenetic gut microbiota distribution and intestinal barrier structure and protection in C57BL/6 mice. Forty adult male mice were divided into four nutritional groups, where the letters refer to the type of diet (control and HFD or HF) and the numbers refer to the period (in weeks) of diet administration: Control diet for 10 wk, HFD for 10 wk, control diet for 16 wk, and HFD for 16 wk. After sacrifice, biochemical, molecular, and stereological analyses were performed. The HF groups were overweight, had gut dysbiosis, had a progressive decrease in occludin immunostaining, and had increased LPS concentrations. Dietary progression reduced the number of goblet cells per large intestine area and Mucin2 expression in the HF16 group, consistent with a completely disarranged intestinal ultrastructure after 16 wk of HFD intake. Chronic HFD intake causes overweight, gut dysbiosis, and morphological and functional alterations of the intestinal barrier after 10 or 16 wk. Time-dependent reductions in goblet cell numerical density and mucus production have emerged as targets for countering obesity-driven intestinal damage.