Low-fat Diet Research Articles

Abstract Mo132: Pouring Salt in the Wound: Sex-specific Cardiometabolic Responses to Increased Dietary Fat, Sugar, and Salt.

Introduction: The general population is becoming more obese, and diabetes rates continue to rise, with overnutrition and consumption of processed foods likely contributing factors. Many people consume diets high in fat, sugar, and salt; however, this triad of factors is rarely examined in unison in studies. In addition, studies that examined diets high in fat and sugar in the context of heart failure with preserved ejection fraction and cardiometabolic outcomes have often performed short dietary interventions, with many studies performed in only male mice, and dietary salt content is often not considered or manipulated. Study Goal: This study aimed to assess the long-term impact of high-fat, high-sucrose diets with differing levels of salt (NaCl) on systemic and cardiovascular physiology in male and female mice. Methods and Results: 12-week-old C57BL/6J male and female mice ( n = 4/group) were fed one of the following diets for 25 weeks: normal chow (NC), low-fat diet (LFD; 10 kcal%), high-fat high sucrose (HFHS; 60 kcal%) with 0.33% NaCl, HFHS with 1% NaCl (HFHS1%), and HFHS with 8% NaCl (HFHS8%). Mice were subjected to basal tail blood metabolite assessment and weighed weekly. In week 24, mice were subjected to glucose tolerance testing, dual-energy X-ray absorptiometry followed by postmortem gravimetric, blood metabolite, histological, and biochemical analyses at 25 weeks. We found that irrespective of sex, body weight was significantly greater in mice receiving HFHS ( p <0.001) and HFHS1% ( p <0.001) versus the other diets. By 25 weeks, male mice were significantly larger than female mice with all diets except HFHS1% ( p <0.05), which correlated with increased percent body fat ( p <0.01), impaired glucose tolerance ( p <0.05) and increased ketone levels ( p <0.05) in female mice subjected to HFHS1% versus males on the same diet. There was also increased heart weight and atrial weights in female mice subjected to HFHS and HFHS1% versus the other females, which was not observed in male mice. Conclusions: Although previous short-term dietary studies have shown that males have altered cardiometabolic responses more than females, our findings together show that long-term dietary interventions with HFHS diets with salt may adversely impact female systemic and cardiovascular physiology.

Histological Analysis of Enamel Microstructure in Response to Dietary Habits: Comparative Study A cross Different Populations

Background: The protective role of enamel against physical and chemical injury is well documented. Despite being classified as connective tissue, with its composition and microstructure dominated by hydroxyapatite crystals it is the hardest in the human body Objective: The purpose of this study is to investigate the histological changes in enamel microstructure that occur when distinct populations follow different food habits. Study Design: This study employs a comparative cross-sectional design. Duration and Place of the Study: This study was conducted at Department of pathology Watim medical and dental college, Rawat , from 3rd June 2022 to 2nd May 2023. Material and Methods: A sum of 300 dental examples were acquired from members having a place with one or the other, High Carbohydrate Diet Group (n=95): people accounting their principle dietary consumption high-carb nourishments like grains/pay/aries and starches. High-Proteins Diet Group (n=108): participants who had the highest consumption of protein-rich foods, such as meat products, legumes and dairy. Mixed Diet Group (n=97): People with intermediate consumptions of carbohydrates, proteins and fats Subsequently, study participants were determined to best represent the two diet groups based on dietary surveys and medical histories. Results: In total, 300 participants are considered in this research, with the mean age of the group on HC totals 3.5 ± 1.3 years, HP group 3.4 ± 9.2 years, and MD group 3.6 ± 1.1 years. The gender distribution also shows similar characteristics, males are 55.8% in HC group, 46.3% in HP group, and 52.6% in MD group; females are 44.2%, 53.7%, and 47.4%, respectively. Concerning the age range, the major cluster is 26-35 years old and 36-45 years old cohorts, which proves the majority of the middle ages. Conclusion: Our results indicate that decomposition is a major factor affecting the surface morphology, structure and health of enamel.

Abstract Tu105: Inhibition of Queuine tRNA-Ribosyltransferase 1 Ameliorates Heaptic Lipogenesis and Atherosclerosis

Background: Atherosclerosis threatens cardiovascular health, which is featured by abnormal lipid metabolism and chronic inflammation in arterial wall. Queuine tRNA-Ribosyltransferase 1 (QTRT1) , is an enzyme responsible for tRNA modification at the wobble base. Research Questions: It is unclear whether the function of QTRT1 is involved in metabolism of non-cancer cells and tissues, especially lipid metabolism mainly orchestrated by liver. Aims: We aimed to explore the role of QTRT1 deficiency in hyperlipidemia, liver steatosis and atherosclerosis. Methods: Transgenic mice such as Qtrt1fl/flAlb-iCre+/- (Qtrt1LKO), Qtrt1fl/fl(WT), ApoE-/-, and gain of function of PCSK9 by adeno-associated virus gene transfer were used to determine the functional significance of QTRT1 in atherosclerosis. Synthesis, transportation and oxidation of lipids in livers and hepatocytes were examined by quantitative real-time polymerase chain reaction. Moreover, primary hepatocytes with overexpression and downregulation of QTRT1 were followed by RNA sequencing to identify downstream targets. Results: Deficiency of hepatic QTRT1 significantly attenuated hyperlipidemia, liver steatosis and atherosclerotic burden, but increased plaque stability in the aorta of mice. Depletion of QTRT1 markedly downregulated de novo lipogenesis (DNL) without influence on lipoprotein transportation and fatty acid oxidation. Qtrt1LKO mice on a high-carbohydrate diet displayed relatively reduced hyperlipidemia and alleviation of DNL. RNA-seq indicated that odorant binding protein 2A (OBP2A) was upregulated in Qtrt1LKO hepatocytes, which reversed the promotion of DNL by QTRT1 in hepatocytes. Conclusion: Inhibition of QTRT1 in hepatocytes ameliorates hepatic lipogenesis and atherosclerosis in mice. Targeting of QTRT1 is a promising strategy to improve therapeutic effectiveness in both hyperlipidemia and atherosclerosis.

Abstract Or123: Increasing ketone supply to the heart has beneficial effects on the source of cardiac ATP production in heart failure with preserved ejection fraction (HFpEF)

Introduction: There is considerable confusion as to what changes in cardiac energy metabolism occur in heart failure with preserved ejection fraction (HFpEF). In HFpEF mice hearts, we found a marked decrease in cardiac glucose oxidation, which is accompanied by an increase in fatty acid oxidation. Ketones have been proposed as an extra source of fuel for the failing, heart, although it remains unclear if ketones may adversely affect glucose and fatty acid oxidation. Methods: 13-month-old C57BL/6N female mice were administered a 60% high-fat diet and L-NAME (0.5g/L/day) for 6 weeks to induce HFpEF. Control mice were fed with regular low-fat diet and regular drinking water. Hearts of the mice were excised and perfused in the isolated working mode aerobically with 5 mM glucose, 0.8 mM palmitate, 100 µU/ml insulin, with either low (0.6 mM) or high (1 mM) levels of β-hydroxybutyrate. Metabolic rates of the hearts were measured with radiolabelled [U- 14 C] glucose, [9,10- 3 H] palmitate, and [3- 14 C] β-hydroxybutyrate. Results: In HFpEF mouse hearts, glucose oxidation was significantly decreased with a parallel increase in fatty acid oxidation. As a result, the HFpEF hearts showed overall preserved ATP production rates (79 ± 12 vs. to 106 ± 13 μmol . g dry wt -1. min -1 control vs. HFpEF). Increasing β-hydroxybutyrate levels from 0.6 mM to 1 mM resulted in a rise in ketone oxidation rates in HFpEF hearts (from 692 ± 47 to 952 ± 90 nmol . g dry wt -1. min -1 ). Interestingly, this increase in ketone oxidation did not further compromise the rates of glucose oxidation in HFpEF hearts, but actually increased glucose oxidation rates (from 95 ± 13 to 190 ± 17 nmol . g dry wt -1. min -1 ), and had minor effects on fatty acid oxidation rates (from 796 ± 123 to 678 ± 92 nmol . g dry wt -1. min -1 ). This resulted in an increase in the contribution of ketone and glucose oxidation to ATP production from 15 % to 28 % in HFpEF hearts. Conclusion: In HFpEF mice hearts overall ATP production is not impaired, but rather the heart switches from glucose oxidation to fatty acid oxidation as the main source of ATP production. Increasing ketone supply to the heart increases ketone oxidation and results in a favourable shift in ATP production in HFpEF.

The Effects of Human Chorionic Gonadotropin and Gonadotropin-Releasing Hormone Receptor Antagonist on Testicular Steroidogenesis in Normal and Obese Rats.

We studied the effect of a high-fat, high-carbohydrate diet (HFHCD) on basal testosterone levels in the blood and testosterone, its precursors, and expression of steroidogenic genes in the testes of rats treated with human chorionic gonadotropin (hCG, 10 IU/rat, subcutaneously, once), gonadotropin-releasing hormone receptor antagonist cetrorelix (75 μg/kg, subcutaneously, 3 days), and their combination. In HFHCD rats, no obvious signs of androgen deficiency were observed and the response of the testes to hCG stimulation was preserved. Unlike control rats (normal diet), the expression of the luteinizing hormone receptor gene in these rats did not change in response to hCG stimulation and cetrorelix administration; they also showed a paradoxical, more pronounced response to hCG administration under conditions of suppression of the gonadotropin secretion by cetrorelix. This suggests that the etiology and pathogenesis of obesity may have different effects on the hormonal status of the male reproductive system.

Characterizing and identifying of miRNAs involved in berberine modulating glucose metabolism of Megalobrama amblycephala.

The present study, as one part of a larger project that aimed to investigate the effects of dietary berberine (BBR) on fish growth and glucose regulation, mainly focused on whether miRNAs involve in BBR's modulation of glucose metabolism in fish. Blunt snout bream Megalobrama amblycephala (average weight of 20.36 ± 1.44g) were exposed to the control diet (NCD, 30% carbohydrate), the high-carbohydrate diet (HCD, 43% carbohydrate) and the berberine diet (HCB, HCD supplemented with 50mg/kg BBR). After 10weeks' feeding trial, intraperitoneal injection of glucose was conducted, and then, the plasma and liver were sampled at 0h, 1h, 2h, 6h, and 12h. The results showed the plasma glucose levels in all groups rose sharply and peaked at 1h after glucose injection. Unlike the NCD and HCB groups, the plasma glucose in the HCD group did not decrease after 1h, while remained high level until at 2h. The NCD group significantly increased liver glycogen content at times 0-2h compared to the other two groups and then liver glycogen decreased sharply until at times 6-12h. To investigate the role of BBR that may cause the changes in plasma glucose and liver glycogen, miRNA high-throughput sequencing was performed on three groups of liver tissues at 2h time point. Eventually, 20 and 12 differentially expressed miRNAs (DEMs) were obtained in HCD vs NCD and HCB vs HCD, respectively. Through function analyzing, we found that HCD may affect liver metabolism under glucose loading through the NF-κB pathway; and miRNAs regulated by BBR mainly play roles in adipocyte lipolysis, niacin and nicotinamide metabolism, and amino acid transmembrane transport. In the functional exploration of newly discovered novel:Chr12_18892, we found its target gene, adenylate cyclase 3 (adcy3), was widely involved in lipid decomposition, amino acid metabolism, and other pathways. Furthermore, a targeting relationship of novel:Chr12_18892 and adcy3 was confirmed by double luciferase assay. Thus, BBR may promote novel:Chr12_18892 to regulate the expression of adcy3 and participate in glucose metabolism.

Association of dietary carbohydrate intake with bone mineral density, osteoporosis and fractures among adults without diabetes: Evidence from National Health and Nutrition Examination Survey

BackgroundThe impact of dietary carbohydrate intake on bone health remains a subject of controversy, potentially influenced by individuals with diabetic osteoporosis who exhibit normal or elevated bone mineral density (BMD). The cross-sectional study was conducted to explore the association between carbohydrate intake and BMD, osteoporosis and fractures among adults without diabetes, based on the National health and nutrition examination survey (NHANES). MethodsParticipants were from the NHANES 2005–2010, excluding individuals with diabetes and those with incomplete data. The association between carbohydrate intake and BMD was analyzed using Spearman correlation, linear regression analysis and subgroup analysis, respectively. The association between carbohydrate intake and osteoporosis/fractures was analyzed using weighted logistic regression analysis. ResultsA total of 7275 adult participants were included and their dietary carbohydrate intake was inversely associated with BMD in the total femur [β = −0.20 95%CI (−0.30, −0.10); p < 0.001], femoral neck [β = −0.10 95%CI (−0.20, −0.00); p = 0.002], and lumbar spine [β = −0.10 95%CI (−0.20, −0.00); p = 0.004]. Stratified analysis indicated that individuals aged 65 and over, women, and non-Hispanic whites were more likely to have lower BMD. Furthermore, a higher intake of dietary carbohydrates was associated with an increased risk of osteoporosis [OR = 1.001 95%CI (1.001, 1.001); p < 0.001] and fractures at the hip [OR = 1.005 95%CI (1.005, 1.005); p < 0.001], wrist [OR = 1.001 95%CI (1.001, 1.001), p < 0.001], and spine [OR = 1.003 95%CI(1.003, 1.003); p < 0.001]. ConclusionsA higher carbohydrate diet is associated with lower BMD and a higher risk of osteoporosis and fractures among adults without diabetes, and a higher carbohydrate consumption show a stronger effect in individuals aged 65 and over, women, and non-Hispanic whites.

A High-Carbohydrate Diet Induces Cognitive Impairment and Promotes Amyloid Burden and Tau Phosphorylation via PI3K/Akt/GSK-3β Pathway in db/db Mice.

Cognitive impairment is a prevalent complication of type 2 diabetes, influenced significantly by various dietary patterns. High-carbohydrate diets (HCDs) are commonly consumed nowadays; however, the specific impact of HCDs on cognitive function in diabetes remains unclear. The objective of this study was to investigate whether an HCD has effects on cognition in diabetes. Eight-week-old diabetic (db/db) mice and wild-type (WT) mice underwent a twelve-week dietary intervention, including a normal diet (ND), an HCD, or a high-fat diet (HFD). Following this, behavioral tests were conducted, and related hippocampal pathology was evaluated. Our results demonstrated that an HCD exacerbated cognitive decline in db/db mice compared to an ND. Additionally, an HCD increased amyloid-β burden and expression of β-site APP cleaving enzyme-1. An HCD was also found to promote the phosphorylation of tau protein via the PI3K/Akt/GSK-3β pathway. Furthermore, an HCD markedly induced neuroinflammation and increased the quantity of microglia and astrocytes. However, these damages induced by an HCD were less severe than those caused by an HFD. Collectively, our findings indicate that a high intake of carbohydrates can have an adverse impact on cognitive function in diabetes.

Unraveling cysteine deficiency-associated rapid weight loss.

Forty percent of the US population and 1 in 6 individuals worldwide are obese, and the incidence of this disease is surging globally1,2. Various dietary interventions, including carbohydrate and fat restriction, and more recently amino acid restriction, have been explored to combat this epidemic3-6. We sought to investigate the impact of removing individual amino acids on the weight profiles of mice. Compared to essential amino acid restriction, induction of conditional cysteine restriction resulted in the most dramatic weight loss, amounting to 20% within 3 days and 30% within one week, which was readily reversed. This weight loss occurred despite the presence of substantial cysteine reserves stored in glutathione (GSH) across various tissues7. Further analysis demonstrated that the weight reduction primarily stemmed from an increase in the utilization of fat mass, while locomotion, circadian rhythm and histological appearance of multiple other tissues remained largely unaffected. Cysteine deficiency activated the integrated stress response (ISR) and NRF2-mediated oxidative stress response (OSR), which amplify each other, leading to the induction of GDF15 and FGF21, hormones associated with increased lipolysis, energy homeostasis and food aversion8-10. We additionally observed rapid tissue coenzyme A (CoA) depletion, resulting in energetically inefficient anaerobic glycolysis and TCA cycle, with sustained urinary excretion of pyruvate, orotate, citrate, α-ketoglutarate, nitrogen rich compounds and amino acids. In summary, our investigation highlights that cysteine restriction, by depleting GSH and CoA, exerts a maximal impact on weight loss, metabolism, and stress signaling compared to other amino acid restrictions. These findings may pave the way for innovative strategies for addressing a range of metabolic diseases and the growing obesity crisis.

Associations between Long-Term Dietary Coenzyme Q10 Intake and New-Onset Hypertension in Adults: Insights from a Nationwide Prospective Cohort Study.

Coenzyme Q10 (CoQ10) supplementation appears to be associated with a lower blood pressure. Nevertheless, it remains unclear whether food-sourced CoQ10 will affect new-onset hypertension in general adults. This study investigated the relationship between dietary CoQ10 intake and new-onset hypertension among the general population. Participants without hypertension at baseline from the China Health and Nutrition Survey (CHNS) prospective cohort study were included (n = 11,428). Dietary CoQ10 intake was collected by validated dietary recalls and the food weighing method. Linear and non-linear relationships between dietary CoQ10 intake and new-onset hypertension were analyzed using multivariable Cox proportional hazards models and restricted cubic splines. During follow-up (median: 6 years), 4006 new-onset hypertension cases were documented. Compared with non-consumers, the hazard ratio (HR) and 95% confidence interval (CI) from quintile 2 to 4 total dietary CoQ10 were 0.83 (0.76, 0.91), 0.86 (0.78, 0.94) and 1.01 (0.92, 1.11); total plant-derived CoQ10 were 0.80 (0.73, 0.88), 1.00 (0.91, 1.09) and 1.10 (1.00, 1.20); and animal-derived CoQ10 were 0.65 (0.59, 0.71), 0.58 (0.53, 0.64) and 0.68 (0.62, 0.75). The lowest risk was found at moderate intake, with a non-linear relationship (P nonlinearity < 0.05). Furthermore, the overall inverse association was stronger among individuals without alcohol consumption or eating a low-fat diet. Moderate long-term dietary CoQ10 intake might be protective against new-onset hypertension. However, it follows a non-linear relationship and excessive intake may increase the risk of new-onset hypertension in the Chinese population.

Yinchenhao Decoction mitigates intestinal impairment induced by high carbohydrate diet in largemouth bass (Micropterus salmoides): insights from inflammation, apoptosis, oxidative stress, tight junctions, and microbiota homeostasis.

As a major source of energy, carbohydrates have a protein-saving effect. However, excessive consumption of carbohydrates can lead to the disruption of the intestinal barrier in fish, especially for carnivorous fish. Therefore, traditional Chinese medicine component Yinchenhao Decoction (YD), was used to detect the effect on intestinal barriers and microbial community equilibrium for largemouth bass in current research. In this research, a series of NC (normal carbohydrate diet) and HC (high carbohydrate diet) with graded YD treatments during 10 weeks feeding trial. Results suggested that 2% and 4% YD treatments significantly reduced gut inflammation and mucosal loss caused by HC. Compared with NC, HC significantly decreased the relative expression of intestinal tight junction-related genes (zo1, claudin1, claudin7, and occludin). However, with the application of YD, the expression of tight junction-related genes (zo1, claudin1, and claudin7) increased significantly (p < 0.05). Likewise, administration of YD significantly reduced elevated plasma diamine oxidase (DAO) activity caused by HC (p < 0.05). Additionally, YD significantly downregulated the mRNA expression of endoplasmic reticulum stress (ERS)-related genes (grp78, atf6, chopα, ire1, xbp1, and eifα) and pro-apoptosis genes (casp3, casp8, and bax) (p < 0.05), while upregulating the anti-apoptosis gene bcl2 (p < 0.05). Moreover, YD significantly increased the mRNA expression of antioxidant genes and the enzyme activities of CAT and GPX, while decreased MDA concentration significantly (p < 0.05). Whereas, YD markedly decreased the expression of pro-inflammatory genes (il1β, tnfα, il8, and nf-κB) and the immune enzymes activity (ACP and AKP) (p < 0.05) by up-regulating the expression of anti-inflammatory genes (ikb and il10). Notably, YD modulated the largemouth bass intestinal microbial community, enhanced the diversity and increased the abundance of probiotic microorganisms in the intestinal microbiota. In summary, YD supplementation in HC alleviated inflammation, apoptosis, oxidative stress, tight-junction injury, and microbiota disequilibrium in the intestine, which suggested that YD could be a valuable functional additive in aquaculture.

Standardized Nutritional Care Process in Type 2 Diabetes Mellitus Patients with Stroke: Low Carbohydrate, Fat and Salt Diet

Diabetes Melitus merupakan salah satu penyakit tidak menular dengan proporsi tertinggi di Indonesia. Menurut data Riskesdas 2018, preval__ensi diabetes mellitus terus mengalami peningkatan. Pengaturan Peningkatan kadar glukosa dapat menimbulkan risiko kerusakan mikrovaskular (retinopati, nefropati, dan neuropati) serta dapat menimbulkan penyakit kardiovaskular, stroke, pembuluh darah perifer dan penurunan kualitas hidup. Empat pilar utama penatalaksanaan diabetes melitus meliputi edukasi, diet, latihan jasmani/aktivitas fisik dan obat. Penatalaksanaan diet pasien diabetes melitus dilakukan melalui serangkaian proses asuhan gizi dan intervensi menganut prinsip 3J (Jenis, Jumlah, Jadwal). Penatalaksanaan diet diharapkan dapat membantu proses penyembuhan penyakit pasien dan mencegah komplikasi. 3 pasien menderita penyakit Diabetes mellitus dengan komplikasi stroke mengalami masalah gizi asupan makanan peroral kurang dari kebutuhan dan kurang pengetahuan selama rawat inap dengan diagnosis DM type 2 dan stroke. Pemberian diet Rendah Karbohidrat , Rendah lemak serta Rendah garam dalam bentuk bervariasi baik jenis maupun bentuk makanannya sesuai dengan kemampuan dan daya terima pasien dilakukan agar terjadi peningkatan asupan. Kolaborasi dilakukan bersama dokter penanggungjawab untuk setiap tindakan yang dilakukan . Edukasi dilakukan untuk meningkatkan pemahaman keluarga dan pasien dan memberikan motivasi kepada keluarga pasien agar setelah di rawat di rumah sakit dapat mempertahankan kesehatannya. Hasil : Intervensi yang diberikan dapat memperbaiki masalah gizi pada pasien Diabetes mellitus dengan komplikasi stroke dan hipertensi

Carbohydrate Intake Levels and the Risk of Metabolic Syndrome in Korean Populations: A Prospective Study.

In Korea and other Asian countries, traditional high-carbohydrate diets are increasingly associated with metabolic syndrome (MetS) and its complications. As dietary patterns shift, there is a growing need to assess the effect of these changes on health outcomes related to MetS. This study aimed to investigate the prospective relationship between carbohydrate consumption and the risk of MetS and its components. We analyzed data from 7902 participants from the Korean Association Resource, part of the Korean Genome and Epidemiology Study Dietary intakes, including carbohydrates and fiber, were assessed using a validated semi-quantitative food frequency questionnaire, allowing for the calculation of the proportion of total energy from carbohydrates (P_CARB) and the carbohydrate-to-fiber ratio to assess carbohydrate quality. Blood samples were collected after at least eight hours of fasting for laboratory analysis. We employed Cox proportional hazards models to estimate hazard ratios and 95% confidence intervals, focusing on the relationship between the P_CARB and the risk of developing MetS and its individual components, while adjusting for carbohydrate quality. In the fully adjusted model, which accounted for carbohydrate quality as a covariate, individuals in the highest percentile of the P_CARB showed a significantly increased risk of MetS, hypertriglyceridemia, hypo-high density lipoprotein cholesterolemia, dyslipidemia, and high blood pressure, compared to those in the lowest P_CARB group. Spline curve analyses indicated that the risks for MetS and its components consistently escalated with increasing P_CARB, with all p-values for nonlinearity exceeding 0.05. The findings suggest that higher levels of P_CARB are associated with an increased risk of MetS and related conditions, except for high fasting glucose. These results highlight the importance of dietary awareness and potential adjustments for populations consuming high-carbohydrate diets.

Beneficial effects of extra virgin olive oil on type 2 diabetes

In contemporary society, chronic diseases become increasingly prevalent, among which is type 2 diabetes. Nowadays, daily diet is gaining growing attention and interest from the general public for its potential to prevent and improve these diseases. One of the ingredients highly recommended to be included in peoples diet is extra virgin olive oil (EVOO), since substantial evidence has shown that it is helpful in reducing body weight and the risk of obesity and type 2 diabetes. Consequently, this review paper is aimed at comparing EVOO with other types of oil or low-fat diets and summarizing its health benefits to type 2 diabetes by analyzing relevant parameters, including fasting blood glucose (FBG), insulin, glycated hemoglobin (HbA1c), body weight, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), etc. A systematic literature search was conducted using Google Scholar with the year range from 2010 to 2023. After being considered against the exclusion criteria, 8 articles were eventually included. Results showed that EVOO is associated with improving some risk factors of diabetes, leading to decreased blood glucose and greater short-term weight loss compared to low-fat diets, and resulting in more body fat loss compared to soybean oil. Thus, EVOO is now expected to be clinically used in treating type 2 diabetes in the future.

Body fat percentage vs body mass index in estimating basal cell carcinoma

BackgroundThe role of body mass index (BMI) in basal cell carcinoma (BCC) risk remains controversial, and limited information is available regarding the relationship between other physical measurements and BCC. Several recent studies have found a positive effect of adiposity on improved survival when obesity was determined solely by BMI (the "obesity paradox"). We hypothesize that body fat percentage (BFP) may serve as a more sensitive risk factor for BCC than BMI. MethodsThe study conducted a retrospective analysis of clinical data from two distinct centers in China. Individual patient-level data were obtained from medical record reviews spanning January 1, 2015, to December 31, 2022. Associations with outcomes were analyzed using univariate and stratified analyses and assessed using multiple logistic regression with adjustment for confounding factors. Additionally, we performed a meta-analysis to further test the observations in our study. ResultsA total of 337 patients, ranging in age from 50 to 91 years, with a mean age of 66.88 (standard deviation 10.16), were included. We observed no significant association between BMI and BCC after adjusting for confounders (OR: 0.71, 95 % CI: 0.36–1.40, P = 0.3186). There was also no convincing effect in a meta-analysis (n = 158,741) (OR: 0.99, 95 % CI: 0.93–1.06, P = 0.8). Furthermore, BFP was found to be associated with BCC (OR: 2.64, 95 % CI: 1.17–5.97, P = 0.0196), supported by strong clinical evidence. ConclusionsOur study supports the hypothesis that BFP is superior to BMI in assessing BCC risk. Multiple logistic regression analyses, coupled with meta-analysis, provided robust evidence that BFP is a sensitive risk factor for BCC, while BMI appears unrelated to risk. According to these findings, routine healthcare practices could benefit from utilizing BFP measurements. The reduction of body fat percentage in low-fat diets may be beneficial for adjuvant treatment of BCC.

Manipulation of feeding patterns in high fat diet fed rats improves microbiota composition dynamics, inflammation and gut-brain signaling

Chronic consumption of high fat (HF) diets has been shown to increase meal size and meal frequency in rodents, resulting in overeating. Reducing meal frequency and establishing periods of fasting, independently of caloric intake, may improve obesity-associated metabolic disorders. Additionally, diet-driven changes in microbiota composition have been shown to play a critical role in the development and maintenance of metabolic disorders. In this study, we used a pair-feeding paradigm to reduce meal frequency and snacking episodes while maintaining overall intake and body weight in HF fed rats. We hypothesized that manipulation of feeding patterns would improve microbiota composition and metabolic outcomes. Male Wistar rats were placed in three groups consuming either a HF, low fat diet (LF, matched for sugar), or pair-fed HF diet for 7 weeks (n = 11–12/group). Pair-fed animals received the same amount of food consumed by the HF fed group once daily before dark onset (HF-PF). Rats underwent oral glucose tolerance and gut peptide cholecystokinin sensitivity tests. Bacterial DNA was extracted from the feces collected during both dark and light cycles and sequenced via Illumina MiSeq sequencing of the 16S V4 region. Our pair-feeding paradigm reduced meal numbers, especially small meals in the inactive phase, without changing total caloric intake. This shift in feeding patterns reduced relative abundances of obesity-associated bacteria and maintained circadian fluctuations in microbial abundances. These changes were associated with improved gastrointestinal (GI) function, reduced inflammation, and improved glucose tolerance and gut to brain signaling. We concluded from these data that targeting snacking may help improve metabolic outcomes, independently of energy content of the diet and hyperphagia.

Hepatic stearoyl-CoA desaturase-1 deficiency induces fibrosis and hepatocellular carcinoma-related gene activation under a high carbohydrate low fat diet

Stearoyl-CoA desaturase-1 (SCD1) is a pivotal enzyme in lipogenesis, which catalyzes the synthesis of monounsaturated fatty acids (MUFA) from saturated fatty acids, whose ablation downregulates lipid synthesis, preventing steatosis and obesity. Yet deletion of SCD1 promotes hepatic inflammation and endoplasmic reticulum stress, raising the question of whether hepatic SCD1 deficiency promotes further liver damage, including fibrosis. To delineate whether SCD1 deficiency predisposes the liver to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC), we employed in vivo SCD1 deficient global and liver-specific mouse models fed a high carbohydrate low-fat diet and in vitro established AML12 mouse cells. The absence of liver SCD1 remarkably increased the saturation of liver lipid species, as indicated by lipidomic analysis, and led to hepatic fibrosis. Consistently, SCD1 deficiency promoted hepatic gene expression related to fibrosis, cirrhosis, and HCC. Deletion of SCD1 increased the circulating levels of Osteopontin, known to be increased in fibrosis, and alpha-fetoprotein, often used as an early marker and a prognostic marker for patients with HCC. De novo lipogenesis or dietary supplementation of oleate, an SCD1-generated MUFA, restored the gene expression related to fibrosis, cirrhosis, and HCC. Although SCD1 deficient mice are protected against obesity and fatty liver, our results show that MUFA deprivation results in liver injury, including fibrosis, thus providing novel insights between MUFA insufficiency and pathways leading to fibrosis, cirrhosis, and HCC under lean non-steatotic conditions.

Effects of Age and Diet on Triglyceride Metabolism in Mice.

Both age and diet can contribute to alterations in triglyceride metabolism and subsequent metabolic disease. In humans, plasma triglyceride levels increase with age. Diets high in saturated fats can increase triglyceride levels while diets high in omega-3 fatty acids decrease triglyceride levels. Here we asked how age and long-term diet effected triglyceride metabolism in mice. We fed male and female mice a low-fat diet, a western diet, or a diet high in polyunsaturated and omega-3 (n-3) fatty acids for up to 2 years. We measured survival, body composition, plasma triglyceride levels, chylomicron clearance, and oral fat, glucose, and insulin tolerance. Triglyceride levels in mice did not increase with age, regardless of diet. Oral fat tolerance increased with age, while chylomicron clearance remained unchanged. Mice fed western diet had decreased survival. Interestingly, mice fed the n-3 diet gained more lean mass, and had lower insulin levels than mice fed either low-fat or western diet. Moreover, triglyceride uptake into the hearts of mice fed the n-3 diet was strikingly higher than in other groups. In mice, age-induced changes in triglyceride metabolism did not match those in humans. Our data suggested that mice, like humans, had decreased fat absorption with age, but plasma triglyceride clearance did not decrease with age in mice, resulting in lower plasma triglyceride levels and improved oral fat tolerance with age. A chronic diet high in n-3 fatty acids increased insulin sensitivity and uptake of triglycerides specifically into the heart but how these observations are connected is unclear. The changes in triglyceride metabolism that occur with age in humans are not reflected in a mouse model, thus mice are likely not an ideal model for understanding how age impacts lipid metabolism and subsequent metabolic disease.A fish-oil based high-fat diet high in omega-3 fatty acids significantly increases fatty acid uptake in the heart while at the same time decreases fasting insulin levels.In future studies it will be important to understand how the omega-3 fatty acid induced increase in fatty acid uptake affects cardiac function and how it is related to other phenotypes induced by omega-3 fatty acids.

Is There an Ideal Diet? Some Insights from the POUNDS Lost Study.

Diets for weight loss have a long history but an ideal one has not yet been clearly identified. To compare low-fat and lower carbohydrate diets, we designed The Preventing Overweight by Novel Dietary Strategies (POUNDS) Lost study. This is a 2 × 2 factorial study with diets of 20% or 40% fat and 15% or 25% protein with a graded carbohydrate intake of 35, 45, 55 and 65%. Weight loss, overall, was modest at nearly 6% with all four diets, and no significant dietary difference. The variability in weight loss in each diet group was significant, ranging from greater than 20% to a small weight gain. Studies of genetic variations in relation to weight loss showed that the diet that was selected could significantly affect weight loss, emphasizing that there is no ideal diet and more than one diet can be used to treat obesity. Weight loss was also influenced by the level of baseline triiodothyronine or thyroxine, and baseline carbohydrate and insulin resistance. Achieving a stable Health Eating Food Diversity Index, eating more protein, eating more fiber, engaging in more physical activity, sleeping better and eating less ultra-processed foods were beneficial strategies for weight loss in this trial. Although there is no "ideal diet", both the DASH diet and the Mediterranean diet have clinical trials showing their significant benefit for cardiovascular risk factors. Finally, the lesson of the "Last Chance Diet", which recommended a diet with protein from gelatin, proved that some diets could be hazardous.

The Effect of Maternal High-Fat or High-Carbohydrate Diet during Pregnancy and Lactation on Cytochrome P450 2D (CYP2D) in the Liver and Brain of Rat Offspring.

Cytochrome P450 2D (CYP2D) is important in psychopharmacology as it is engaged in the metabolism of drugs, neurosteroids and neurotransmitters. An unbalanced maternal diet during pregnancy and lactation can cause neurodevelopmental abnormalities and increases the offspring's predisposition to neuropsychiatric diseases. The aim of the present study was to evaluate the effect of maternal modified types of diet: a high-fat diet (HFD) and high-carbohydrate diet (HCD) during pregnancy and lactation on CYP2D in the liver and brain of male offspring at 28 (adolescent) or 63 postnatal days (young adult). The CYP2D activity and protein level were measured in the liver microsomes and the levels of mRNAs of CYP2D1, 2D2 and 2D4 were investigated both in the liver and brain. In the liver, both HFD and HCD increased the mRNA levels of all the three investigated CYP2D genes in adolescents, but an opposite effect was observed in young adults. The CYP2D protein level increased in adolescents but not in young adults. In contrast, young adults showed significantly decreased CYP2D activity. Similar effect of HFD on the CYP2D mRNAs was observed in the prefrontal cortex, while the effect of HCD was largely different than in the liver (the CYP2D2 expression was not affected, the CYP2D4 expression was decreased in young adults). In conclusion, modified maternal diets influence the expression of individual CYP2D1, CYP2D2 and CYP2D4 genes in the liver and brain of male offspring, which may affect the metabolism of CYP2D endogenous substrates and drugs and alter susceptibility to brain diseases and pharmacotherapy outcome.