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Cell Metabolism Oct 2022Bile acids (BAs) are complex and incompletely understood enterohepatic-derived hormones that control whole-body metabolism. Here, we profiled postprandial BAs in the...
Bile acids (BAs) are complex and incompletely understood enterohepatic-derived hormones that control whole-body metabolism. Here, we profiled postprandial BAs in the liver, feces, and plasma of 360 chow- or high-fat-diet-fed BXD male mice and demonstrated that both genetics and diet strongly influence BA abundance, composition, and correlation with metabolic traits. Through an integrated systems approach, we mapped hundreds of quantitative trait loci that modulate BAs and identified both known and unknown regulators of BA homeostasis. In particular, we discovered carboxylesterase 1c (Ces1c) as a genetic determinant of plasma tauroursodeoxycholic acid (TUDCA), a BA species with established disease-preventing actions. The association between Ces1c and plasma TUDCA was validated using data from independent mouse cohorts and a Ces1c knockout mouse model. Collectively, our data are a unique resource to dissect the physiological importance of BAs as determinants of metabolic traits, as underscored by the identification of CES1C as a master regulator of plasma TUDCA levels.
Topics: Animals; Bile Acids and Salts; Carboxylic Ester Hydrolases; Diet, High-Fat; Homeostasis; Hormones; Liver; Male; Mice; Systems Analysis; Taurochenodeoxycholic Acid
PubMed: 36099916
DOI: 10.1016/j.cmet.2022.08.015 -
Ageing Research Reviews Nov 2022Amyloid beta (Aβ) is a peptide and a hallmark of Alzheimer's disease (AD). Emerging evidence suggests that Aβ levels could be influenced by diet. However, the evidence... (Review)
Review
Amyloid beta (Aβ) is a peptide and a hallmark of Alzheimer's disease (AD). Emerging evidence suggests that Aβ levels could be influenced by diet. However, the evidence is sparse and for some nutrients, controversial. The aim of this narrative review is to gather the findings of observational and clinical trials involving human participants on the relationships between nutrients and brain Aβ status. Some dietary patterns are associated to reduced levels of Aβ in the brain, such as the Mediterranean diet, ketogenic diet as well as low intake of saturated fat, high-glycemic-index food, sodium, and junk/fast food. Low Aβ status in the brain was also associated with higher density lipoproteins (HDL) cholesterol and polyunsaturated fatty acids consumption. Data on alcohol intake is not conclusive. On the contrary, high Aβ levels in the brain were related to a higher intake of total cholesterol, triglycerides, low-density lipoproteins (LDL) cholesterol, saturated fat, sucrose, and fructose. Folic acid, cobalamin, vitamin E, and vitamin D were not associated to Aβ status, while high blood concentrations of Calcium, Aluminum, Zinc, Copper, and Manganese were associated with decreased Aβ blood levels but were not associated with Aβ cerebral spinal fluid (CSF) concentrations. In conclusion, certain dietary patterns and nutrients are associated to brain Aβ status. Further research on the association between nutrients and brain Aβ status is needed in order to pave the way to use nutritional interventions as efficacious strategies to prevent Aβ disturbance and potentially AD.
Topics: Aluminum; Alzheimer Disease; Amyloid beta-Peptides; Brain; Calcium; Cholesterol; Copper; Diet, Mediterranean; Fatty Acids; Fatty Acids, Unsaturated; Folic Acid; Fructose; Humans; Lipoproteins, LDL; Manganese; Sodium; Sucrose; Triglycerides; Vitamin B 12; Vitamin D; Vitamin E; Vitamins; Zinc
PubMed: 36049590
DOI: 10.1016/j.arr.2022.101728 -
Nutrients Dec 2022Quantitative rankings of multiple dietary patterns for their effects on non-communicable disease (NCD) biomarkers is lacking and would inform primary prevention... (Meta-Analysis)
Meta-Analysis Review
Quantitative rankings of multiple dietary patterns for their effects on non-communicable disease (NCD) biomarkers is lacking and would inform primary prevention strategies. Accordingly, a network meta-analysis (NMA) was conducted to compare and rank the effects of different dietary patterns on NCD biomarkers, and associations of dietary patterns’ underlying macronutrient composition with NCD biomarkers were determined by a nutritional geometry approach. Randomised controlled trials (RCTs) were eligible for inclusion if they enrolled healthy participants, employed food-based dietary pattern interventions without energy restriction, and reported NCD biomarker outcomes. NCD biomarkers were included as an outcome if ≥10 trials were available. A systematic search of five electronic databases identified 4008 records. Sixty-eight articles from 59 RCTs reporting lipids, glycemic, and inflammatory biomarkers were included for quantitative syntheses. Risk-of-bias was predominantly categorized as low or having some concerns, and confidence-of-evidence low. Relative to western habitual diet, the Mediterranean, Dietary Approaches to Stop Hypertension (DASH), dietary guidelines-based, plant-based, and low-fat diets reduced low-density lipoprotein cholesterol (mean difference range: −0.29 to −0.17 mmol/L), total cholesterol (−0.36 to −0.24 mmol/L), and apolipoprotein B (−0.11 to −0.07 g/L) (all p < 0.05); the Paleo, plant-based and dietary guidelines-based diets reduced homeostasis model assessment of insulin resistance (−0.95 to −0.35, all p < 0.05). No dietary pattern ranked consistently highest. The Paleo diet received the highest all-outcomes-combined average Surface Under the Cumulative Ranking Curve value (67%), followed by DASH (62%) and Mediterranean diets (57%), whereas western habitual diet was lowest (36%). Our findings were independent of macronutrient composition, highlighting the significance of dietary pattern-level analysis.
Topics: Humans; Noncommunicable Diseases; Network Meta-Analysis; Cholesterol, LDL; Diet, Mediterranean; Diet, Fat-Restricted
PubMed: 36615733
DOI: 10.3390/nu15010076 -
Archives of Endocrinology and Metabolism Apr 2022Dietary cholesterol is absorbed in proportion to the amount ingested, blocking its hepatic synthesis, increasing its biliary excretion, only slightly increasing... (Review)
Review
Dietary cholesterol is absorbed in proportion to the amount ingested, blocking its hepatic synthesis, increasing its biliary excretion, only slightly increasing production of bile acids while potentially raising the serum concentration of the atherogenic low-density lipoprotein. Humans lie midway between rats and rabbits that respond to dietary cholesterol, respectively, with high and low capacity to produce bile acids, and low or high capacity to raise blood cholesterol. There are regular studies exonerating as well as blaming dietary cholesterol as a cardiovascular risk factor, particularly in genetic hypercholesterolemic individuals. We then resorted at reviewing all meta-analyses on the subject but failed to reach at a clear conclusion useful in medical practice. Nevertheless, ingestion of the same amount of cholesterol results in wide variation in the amounts absorbed and in plasma lipoprotein profiles depending on poorly understood genetic factors. Several genetic conditions are capable of interfering with the absorption and synthesis of cholesterol. Hyperabsorption of dietary cholesterol elicits the accumulation of cholesterol in the liver and in plasma. In this regard, most cases of familial hypercholesterolemia that have a case of intestinal hyperabsorption of cholesterol also demonstrate the same defect. A practical useful suggestion is to measure for a few weeks the total serum cholesterol and its fractions at least three times before and during the intake of eggs that the candidate wishes to maintain in his usual dietary practice as an efficient procedure to identify those who respond with undesirable increases in serum cholesterol.
Topics: Animals; Bile Acids and Salts; Cholesterol; Cholesterol, Dietary; Diet; Humans; Lipoproteins; Liver; Rabbits; Rats
PubMed: 35420270
DOI: 10.20945/2359-3997000000464 -
Current Atherosclerosis Reports Feb 2022An abnormal lipid profile is considered a main risk factor for cardiovascular diseases and evidence suggests that single nucleotide polymorphisms (SNPs) in the... (Review)
Review
PURPOSE OF REVIEW
An abnormal lipid profile is considered a main risk factor for cardiovascular diseases and evidence suggests that single nucleotide polymorphisms (SNPs) in the cholesteryl ester transfer protein (CETP) gene contribute to variations in lipid levels in response to dietary intake. The objective of this review was to identify and discuss nutrigenetic studies assessing the interactions between CETP SNPs and dietary factors on blood lipids.
RECENT FINDINGS
Relevant articles were obtained through a literature search of PubMed and Google Scholar through to July 2021. An article was included if it examined an interaction between CETP SNPs and dietary factors on blood lipids. From 49 eligible nutrigenetic studies, 27 studies reported significant interactions between 8 CETP SNPs and 17 dietary factors on blood lipids in 18 ethnicities. The discrepancies in the study findings could be attributed to genetic heterogeneity, and differences in sample size, study design, lifestyle and measurement of dietary intake. The most extensively studied ethnicities were those of Caucasian populations and majority of the studies reported an interaction with dietary fat intake. The rs708272 (TaqIB) was the most widely studied CETP SNP, where 'B1' allele was associated with higher CETP activity, resulting in lower high-density lipoprotein cholesterol and higher serum triglycerides under the influence of high dietary fat intake. Overall, the findings suggest that CETP SNPs might alter blood lipid profiles by modifying responses to diet, but further large studies in multiple ethnic groups are warranted to identify individuals at risk of adverse lipid response to diet.
Topics: Cholesterol Ester Transfer Proteins; Cholesterol, HDL; Diet; Dietary Fats; Genotype; Humans; Lipids; Nutrigenomics
PubMed: 35098451
DOI: 10.1007/s11883-022-00987-y -
Current Opinion in Insect Science Feb 2021Temporal patterning of neural progenitors, in which different factors are sequentially expressed, is an evolutionarily conserved strategy for generating neuronal... (Review)
Review
Temporal patterning of neural progenitors, in which different factors are sequentially expressed, is an evolutionarily conserved strategy for generating neuronal diversity during development. In the Drosophila embryo, mechanisms that mediate temporal patterning of neural stem cells (neuroblasts) are largely cell-intrinsic. However, after embryogenesis, neuroblast temporal patterning relies on extrinsic cues as well, as freshly hatched larvae seek out nutrients and other key resources in varying natural environments. We recap current understanding of neuroblast-intrinsic temporal programs and discuss how neuroblast extrinsic cues integrate and coordinate with neuroblast intrinsic programs to control numbers and types of neurons produced. One key emerging extrinsic factor that impacts temporal patterning of neuroblasts and their daughters as well as termination of neurogenesis is the steroid hormone, ecdysone, a known regulator of large-scale developmental transitions in insects and arthropods. Lastly, we consider evolutionary conservation and discuss recent work on thyroid hormone signaling in early vertebrate brain development.
Topics: Animals; Biological Evolution; Diet; Drosophila melanogaster; Ecdysone; Neural Stem Cells; Neurogenesis; Signal Transduction; Thyroid Hormones; Vertebrates
PubMed: 33127508
DOI: 10.1016/j.cois.2020.10.008 -
Clinical Endocrinology Nov 2020To assess the influence of a dietary sodium intake intervention on cortisol measurements within the general population.
OBJECTIVES
To assess the influence of a dietary sodium intake intervention on cortisol measurements within the general population.
DESIGN
Cross-over intervention.
PATIENTS
Six hundred thirty adults without known Cushing syndrome, cardiovascular or renal disease completed a restricted dietary sodium diet (10 mmol/d, 230 mg/d) followed by cross-over to a liberalized dietary sodium diet (200 mmol/d, 4600 mg/d). Twenty-four-hour urine collection and biochemical investigations were performed at the end of each dietary intervention.
RESULTS
Mean 24-hour urinary free cortisol increased with liberalized sodium intake when compared with restricted sodium intake (178.0 ± 89.7 vs 121.3 ± 65.6 nmol/d, P < .001). Nearly all participants (84%) had an increase in the urinary free cortisol following liberalized sodium intake. This translated to a substantial difference in the proportion of participants exceeding categorical thresholds of urinary cortisol on liberalized vs restricted sodium intake: 62% vs 27% for 138 nmol/d (50 mcg/d), 46% vs 17% for 166 nmol/d (60 mcg/d), 32% vs 10% for 193 nmol/d (70 mcg/d), 23% vs 6% for 221 nmol/d (80 mcg/d), 17% vs 4% for 248 nmol/d (90 mcg/d). In parallel, there was a small decrease in morning total serum cortisol with liberalized sodium intake (303.0 ± 117.3 vs 326.4 ± 162.5 nmol/L, P < .001).
CONCLUSIONS
Increased dietary sodium intake increases urinary free cortisol excretion and may increase the risk for false-positive results. Variations in dietary sodium intake may influence the interpretations of cortisol measurements performed to evaluate for hypercortisolism.
Topics: Adult; Cushing Syndrome; Diet; Humans; Hydrocortisone; Nutritional Status; Sodium, Dietary
PubMed: 32511774
DOI: 10.1111/cen.14262 -
Microbiome May 2023The Western dietary pattern, characterized by high consumption of fats and sugars, has been strongly associated with an increased risk of developing Crohn's disease...
BACKGROUND
The Western dietary pattern, characterized by high consumption of fats and sugars, has been strongly associated with an increased risk of developing Crohn's disease (CD). However, the potential impact of maternal obesity or prenatal exposure to a Western diet on offspring's susceptibility to CD remains unclear. Herein, we investigated the effects and underlying mechanisms of a maternal high-fat/high-sugar Western-style diet (WD) on offspring's susceptibility to 2,4,6-Trinitrobenzenesulfonic acid (TNBS)-induced Crohn's-like colitis.
METHODS
Maternal dams were fed either a WD or a normal control diet (ND) for eight weeks prior to mating and continued throughout gestation and lactation. Post-weaning, the offspring were subjected to WD and ND to create four groups: ND-born offspring fed a normal diet (N-N) or Western diet (N-W), and WD-born offspring fed a normal (W-N) or Western diet (W-W). At eight weeks of age, they were administered TNBS to induce a CD model.
RESULTS
Our findings revealed that the W-N group exhibited more severe intestinal inflammation than the N-N group, as demonstrated by a lower survival rate, increased weight loss, and a shorter colon length. The W-N group displayed a significant increase in Bacteroidetes, which was accompanied by an accumulation of deoxycholic acid (DCA). Further experimentation confirmed an increased generation of DCA in mice colonized with gut microbes from the W-N group. Moreover, DCA administration aggravated TNBS-induced colitis by promoting Gasdermin D (GSDMD)-mediated pyroptosis and IL-1beta (IL-1β) production in macrophages. Importantly, the deletion of GSDMD effectively restrains the effect of DCA on TNBS-induced colitis.
CONCLUSIONS
Our study demonstrates that a maternal Western-style diet can alter gut microbiota composition and bile acid metabolism in mouse offspring, leading to an increased susceptibility to CD-like colitis. These findings highlight the importance of understanding the long-term consequences of maternal diet on offspring health and may have implications for the prevention and management of Crohn's disease. Video Abstract.
Topics: Humans; Pregnancy; Female; Mice; Animals; Crohn Disease; Diet, Western; Prenatal Exposure Delayed Effects; Colitis; Diet, High-Fat; Deoxycholic Acid; Mice, Inbred C57BL
PubMed: 37131223
DOI: 10.1186/s40168-023-01546-6 -
The Journal of Clinical Endocrinology... Nov 2023Childhood overweight has been linked to earlier development of adrenarche and puberty, but it remains unknown if lifestyle interventions influence sexual maturation in...
CONTEXT
Childhood overweight has been linked to earlier development of adrenarche and puberty, but it remains unknown if lifestyle interventions influence sexual maturation in general populations.
OBJECTIVE
To investigate if a 2-year lifestyle intervention influences circulating androgen concentrations and sexual maturation in a general population of children.
METHODS
We conducted a 2-year physical activity and dietary intervention study in which 421 prepubertal and mostly normal-weight 6- to 9-year-old children were allocated either to a lifestyle intervention group (119 girls, 132 boys) or a control group (84 girls, 86 boys). The main outcome measures were serum dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), androstenedione (A4), and testosterone concentrations, and clinical adrenarchal and pubertal signs.
RESULTS
The intervention and control groups had no differences in body size and composition, clinical signs of androgen action, and serum androgens at baseline. The intervention attenuated the increase of DHEA (P = .032), DHEAS (P = .001), A4 (P = .003), and testosterone (P = .007) and delayed pubarche (P = .038) in boys but it only attenuated the increase of DHEA (P = .013) and DHEAS (P = .003) in girls. These effects of lifestyle intervention on androgens and the development of pubarche were independent of changes in body size and composition, but the effects of intervention on androgens were partly explained by changes in fasting serum insulin.
CONCLUSION
A combined physical activity and dietary intervention attenuates the increase of serum androgen concentrations and sexual maturation in a general population of prepubertal and mostly normal-weight children, independently of changes in body size and composition.
Topics: Child; Female; Humans; Male; Adrenarche; Androgens; Androstenedione; Dehydroepiandrosterone; Dehydroepiandrosterone Sulfate; Puberty; Testosterone; Exercise; Diet, Healthy
PubMed: 37329220
DOI: 10.1210/clinem/dgad367 -
Frontiers in Endocrinology 2023Fasting morning cortisol (FMC) stress hormone levels, are suggested to reflect increased cardiometabolic risk. Acute response to weight loss diet could elevate FMC.... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
Fasting morning cortisol (FMC) stress hormone levels, are suggested to reflect increased cardiometabolic risk. Acute response to weight loss diet could elevate FMC. Richer Polyphenols and lower carbohydrates diets could favor FMC levels. We aimed to explore the effect of long-term high polyphenol Mediterranean diet (green-MED) on FMC and its relation to metabolic health.
METHODS
We randomized 294 participants into one of three dietary interventions for 18-months: healthy dietary guidelines (HDG), Mediterranean (MED) diet, and Green-MED diet. Both MED diets were similarly hypocaloric and lower in carbohydrates and included walnuts (28 g/day). The high-polyphenols/low-meat Green-MED group further included green tea (3-4 cups/day) and a Wolffia-globosa Mankai plant 1-cup green shakeFMC was obtained between 07:00-07:30AM at baseline, six, and eighteen-months.
RESULTS
Participants (age=51.1years, 88% men) had a mean BMI of 31.3kg/m, FMC=304.07nmol\L, and glycated-hemoglobin-A1c (HbA1c)=5.5%; 11% had type 2 diabetes and 38% were prediabetes. Baseline FMC was higher among men (308.6 ± 90.05nmol\L) than women (269.6± 83.9nmol\L;p=0.02). Higher baseline FMC was directly associated with age, dysglycemia, MRI-assessed visceral adiposity, fasting plasma glucose (FPG), high-sensitivity C-reactive-protein (hsCRP), testosterone, Progesterone and TSH levels (p ≤ 0.05 for all). The 18-month retention was 89%. After 6 months, there were no significant changes in FMC among all intervention groups. However, after 18-months, both MED groups significantly reduced FMC (MED=-1.6%[-21.45 nmol/L]; Green-MED=-1.8%[-26.67 nmol/L]; p<0.05 vs. baseline), as opposed to HDG dieters (+4%[-12 nmol/L], p=0.28 vs. baseline), whereas Green-MED diet FMC change was significant as compared to HDG diet group (p=0.048 multivariable models). Overall, 18-month decrease in FMC levels was associated with favorable changes in FPG, HbA1c, hsCRP, TSH, testosterone and MRI-assessed hepatosteatosis, and with unfavorable changes of HDLc (p<0.05 for all, weight loss adjusted, multivariable models).
CONCLUSION
Long-term adherence to MED diets, and mainly green-MED/high polyphenols diet, may lower FMC, stress hormone, levels,. Lifestyle-induced FMC decrease may have potential benefits related to cardiometabolic health, irrespective of weight loss.
CLINICAL TRIAL REGISTRATION
ClinicalTrials.gov, identifier NCT03020186.
Topics: Female; Humans; Male; Middle Aged; C-Reactive Protein; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Diet, Mediterranean; Fasting; Glycated Hemoglobin; Hydrocortisone; Testosterone; Thyrotropin; Weight Loss
PubMed: 38034010
DOI: 10.3389/fendo.2023.1243910