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The Mediterranean (MED) diet was associated with a reduced risk of chronic disease, but the epidemiological studies reported inconsistent findings related to the MED diet and non-alcoholic fatty liver disease (NAFLD) risk. This age and the gender-matched case-control study were conducted among 247 adult patients. The MED diet score was obtained based on the Trichopoulou model. Multivariate logistic regression was used to examine the association between the MED diet and NAFLD risk. NAFLD prevalence in people with low, moderate and high adherence to the MED diet was 33, 13⋅1 and 4⋅6 %, respectively. The increasing intake of the MED diet was significantly related to the increment intake of nuts and fruits, vegetables, monounsaturated fatty acid/polyunsaturated fatty acid ratio, legumes, cereals and fish. However, total energy consumption, low-fat dairy and meats intake were reduced (P for all < 0⋅05). Following control for age, the person in the highest of the MED diet tertile compared with the lowest, the odds of NAFLD decreased (OR: 0⋅40, 95 % CI: 0⋅17–0⋅95). This relation became a little stronger after further adjusting for sex, diabetes, physical activity and supplement intake (OR: 0⋅36, 95 % CI: 0⋅15–0⋅89). However, this association disappeared after adjusting for body mass index, waist and hip circumference (OR: 0⋅70, 95 % CI: 0⋅25–1⋅97). High adherence to the MED diet was associated with a 64 % reduction in NAFLD odds before some anthropometric variable adjustments. However, further prospective studies are required, particularly in BMI-stratified models.
Enterohepatic circulation of 12α-hydroxylated (12αOH) bile acid (BA) is enhanced depending on the energy intake in high-fat diet-fed rats. Such BA metabolism can be reproduced using a diet supplemented with cholic acid (CA), which also induces simple steatosis, without inflammation and fibrosis, accompanied by some other symptoms that are frequently observed in the condition of non-alcoholic fatty liver in rats. We investigated whether supplementation of the diet with raffinose (Raf) improves hepatic lipid accumulation induced by the CA-fed condition in rats. After acclimation to the AIN-93-based control diet, male Wistar rats were fed diets supplemented with a combination of Raf (30 g/kg diet) and/or CA (0·5 g/kg diet) for 4 weeks. Dietary Raf normalised hepatic TAG levels (two-way ANOVA P < 0·001 for CA, P = 0·02 for Raf and P = 0·004 for interaction) in the CA-supplemented diet-fed rats. Dietary Raf supplementation reduced hepatic 12αOH BA concentration (two-way ANOVA P < 0·001 for CA, P = 0·003 for Raf and P = 0·03 for interaction). The concentration of 12αOH BA was reduced in the aortic and portal plasma. Raf supplementation increased acetic acid concentration in the caecal contents (two-way ANOVA P = 0·001 as a main effect). Multiple regression analysis revealed that concentrations of aortic 12αOH BA and caecal acetic acid could serve as predictors of hepatic TAG concentration (R2 = 0·55, P < 0·001). However, Raf did not decrease the secondary 12αOH BA concentration in the caecal contents as well as the transaminase activity in the CA diet-fed rats. These results imply that dietary Raf normalises hepatic lipid accumulation via suppression of enterohepatic 12αOH BA circulation.
Sarcopenic obesity is regarded as a risk factor for the progression and development of non-alcoholic fatty liver disease (NAFLD). Since male sex is a risk factor for NAFLD and skeletal muscle mass markedly varies between the sexes, we examined whether sex influences the association between appendicular skeletal muscle mass to visceral fat area ratio (SVR), that is, an index of skeletal muscle mass combined with abdominal obesity, and the histological severity of NAFLD. The SVR was measured by bioelectrical impedance in a cohort of 613 (M/F = 443/170) Chinese middle-aged individuals with biopsy-proven NAFLD. Multivariable logistic regression and subgroup analyses were used to test the association between SVR and the severity of NAFLD (i.e. non-alcoholic steatohepatitis (NASH) or NASH with the presence of any stage of liver fibrosis). NASH was identified by a NAFLD activity score ≥5, with a minimum score of 1 for each of its categories. The presence of fibrosis was classified as having a histological stage ≥1. The SVR was inversely associated with NASH in men (adjusted OR 0·62; 95 % CI 0·42, 0·92, P = 0·017 for NASH, adjusted OR 0·65; 95 % CI 0·43, 0·99, P = 0·043 for NASH with the presence of fibrosis), but not in women (1·47 (95 % CI 0·76, 2·83), P = 0·25 for NASH, and 1·45 (95 % CI 0·74, 2·83), P = 0·28 for NASH with the presence of fibrosis). There was a significant interaction for sex and SVR (Pinteraction = 0·017 for NASH and Pinteraction = 0·033 for NASH with the presence of fibrosis). Our findings show that lower skeletal muscle mass combined with abdominal obesity is strongly associated with the presence of NASH only in men.
Elevated levels of liver enzymes are the main markers of liver dysfunction. Liver enzymes are the important indicators of non-alcoholic fatty liver disease (NAFLD) in the general population. Previous randomised clinical trials (RCT) investigated the effects of Mediterranean diet (MedDiet) as a plant-based diet on features of NAFLD like liver enzymes, but their results are contradictory. This study aimed to systematically review and meta-analyse RCT investigating the effect of MedDiet on liver enzymes. PubMed, Web of Science, Scopus and Google Scholar were searched until December 2020. A total of ten RCT (n 705 participants) evaluating the effect of MedDiet on liver enzymes including aspartate aminotransferase (AST), alanine transaminase (ALT) and γ-glutamyltransferase (GGT) were included. A random effects model was used to estimate the pooled effect size. To evaluate the heterogeneity among the included studies, the Cochran’s Q-test and I-squared test were used. The MedDiet significantly reduced AST (weighted mean difference (WMD) = −0·38 IU/l; 95 % CI − 0·73, −0·03 IU/l; P = 0·03) and GGT (WMD = −0·16 IU/l; 95 % CI − 0·32, −0·006 IU/l; P = 0·04) but had no significant effect on ALT (WMD = −0·55 IU/l; 95 % CI − 1·25, 0·13 IU/l; P = 0·11). However, sensitivity analysis revealed that the overall effects of MedDiet on AST, GGT and ALT were significantly influenced by removing some studies. There was no publication bias based on Begg’s and Egger’s tests. Generally, MedDiet can improve liver enzymes. To better conclusion, further RCT investigating the effect of MedDiet on liver enzymes, especially in patients with NAFLD, are still required.
Maternal obesity increases the risk of nonalcoholic fatty liver disease (NAFLD) in offspring. The Roux-en-Y gastric bypass (RYBG) is effective for achieving weight loss and ameliorates NAFLD. To determine whether these benefits are maintained after pregnancy and/or lactation, and whether they modulate hepatic morphofunction in the next generation, we evaluated hepatic lipid metabolism in Western diet (WD)-obese female rats that underwent RYGB and in their F1 offspring at adulthood. Female Wistar rats consumed a WD from 21 to 130 days of age, before being submitted to RYGB (WD-RYGB-F0) or SHAM (WD-SHAM-F0) operations. After 5 weeks, these females were mated with control male breeders, and the male and female F1 offspring were identified as WD-RYGB-F1 and WD-SHAM-F1. WD-RYGB-F0 dams exhibited lower serum lipids levels, but severe hepatic steatosis and pathological features of advanced liver injury. The hepatic proteins involved in lipogenesis were reduced in WD-RYGB-F0, as were the genes related to β-oxidation and bile acids (BAs). Although the female and male WD-RYGB-F1 groups did not exhibit hepatic steatosis, the livers of female WD-RYGB-F1 demonstrated higher amounts of lipogenic genes and proteins, while male WD-RYGB-F1 presented a similar downregulation of lipogenic factors to that seen in WD-RYGB-F0 dams. In contrast, maternal and offspring groups of both sexes displayed reductions in the expressions of genes involved in BAs physiology and gluconeogenesis. As such, RYGB aggravates NAFLD after pregnancy and lactation and induces a gender-dependent differential expression of the hepatic lipogenesis pathway in offspring, indicating that female WD-RYGB-F1 may be an increased risk of developing NAFLD.
Practice guidelines for non-alcoholic fatty liver disease (NAFLD) recommend promoting the Mediterranean dietary pattern (MDP) which is cardioprotective and may improve hepatic steatosis. This study aimed to explore multidisciplinary clinicians’ perspectives on whether the MDP is recommended in routine management of NAFLD and barriers and facilitators to its implementation in a multi-ethnic setting. Semi-structured individual interviews were conducted with fourteen clinicians (seven doctors, three nurses, three dietitians and one exercise physiologist) routinely managing patients with NAFLD in metropolitan hospital outpatient clinics in Australia. Interviews were audio-recorded, transcribed and analysed using thematic content analysis. Clinicians described that lifestyle modification was their primary treatment for NAFLD and promoting diet was recognised as everyone’s role, whereby doctors and nurses raise awareness and dietitians provide individualisation. The MDP was regarded as the most evidence-based diet choice currently and was frequently recommended in routine care. Facilitators to MDP implementation in practice were: improvement in diet quality as a parallel goal to weight loss; in-depth knowledge of the dietary pattern; access to patient education and monitoring resources and; service culture, including an interdisciplinary clinic goal, and knowledge sharing from expert dietitians. Barriers included perceived challenges for patients from diverse cultural and socio-economic backgrounds and limited clinician training, time and resourcing to support behaviour change. Integration of MDP in routine management of NAFLD in specialist clinics was facilitated by a focus on diet quality, knowledge sharing, belief in evidence and an interdisciplinary team. Innovations to service delivery could better support and empower patients to change dietary behaviour long-term.
Neuropsychiatric disorders are major causes of the global burden of diseases, frequently co-occurring with multiple co-morbidities, especially obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease and its various risk factors in the metabolic syndrome. While the determining factors of neuropsychiatric disorders are complex, recent studies have shown that there is a strong link between diet, metabolic state and neuropsychiatric disorders, including anxiety and depression. There is no doubt that rodent models are of great value for preclinical research. Therefore, this article focuses on a rodent model of chronic consumption of high-fat diet (HFD), and/or the addition of a certain amount of cholesterol or sugar, meanwhile, summarising the pattern of diet that induces anxiety/depressive-like behaviour and the underlying mechanism. We highlight how dietary and metabolic risk influence neuropsychiatric behaviour in animals. Changes in dietary patterns, especially HFD, can induce anxiety- or depression-like behaviours, which may vary by diet exposure period, sex, age, species and genetic background of the animals used. Furthermore, dietary patterns significantly aggravate anxiety/depression-like behaviour in animal models of neuropsychiatric disorders. The mechanisms by which diet induces anxiety/depressive-like behaviour may involve neuroinflammation, neurotransmitters/neuromodulators, neurotrophins and the gut–brain axis. Future research should be focused on elucidating the mechanism and identifying the contribution of diet and diet-induced metabolic risk to neuropsychiatric disorders, which can form the basis for future clinical dietary intervention strategies for neuropsychiatric disorders.
Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver disease that accompanies obesity and the metabolic syndrome. Excess fructose consumption can initiate or exacerbate NAFLD in part due to a consequence of impaired hepatic fructose metabolism. Preclinical data emphasized that fructose-induced altered gut microbiome, increased gut permeability, and endotoxemia play an important role in NAFLD, but human studies are sparse. The present study aimed to determine if two weeks of excess fructose consumption significantly alters gut microbiota or permeability in humans.
We performed a pilot double-blind, cross-over, metabolic unit study in 10 subjects with obesity (body mass index [BMI] 30–40 mg/kg/m2). Each arm provided 75 grams of either fructose or glucose added to subjects’ individual diets for 14 days, substituted isocalorically for complex carbohydrates, with a 19-day wash-out period between arms. Total fructose intake provided in the fructose arm of the study totaled a mean of 20.1% of calories. Outcome measures included fecal microbiota distribution, fecal metabolites, intestinal permeability, markers of endotoxemia, and plasma metabolites.
Routine blood, uric acid, liver function, and lipid measurements were unaffected by the fructose intervention. The fecal microbiome (including Akkermansia muciniphilia), fecal metabolites, gut permeability, indices of endotoxemia, gut damage or inflammation, and plasma metabolites were essentially unchanged by either intervention.
In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD.
The longitudinal relationship between depression and the risk of non-alcoholic fatty liver disease is uncertain. We examined: (a) the association between depressive symptoms and incident hepatic steatosis (HS), both with and without liver fibrosis; and (b) the influence of obesity on this association.
A cohort of 142 005 Korean adults with neither HS nor excessive alcohol consumption at baseline were followed for up to 8.9 years. The validated Center for Epidemiologic Studies-Depression score (CES-D) was assessed at baseline, and subjects were categorised as non-depressed (a CES-D < 8, reference) or depression (CES-D ⩾ 16). HS was diagnosed by ultrasonography. Liver fibrosis was assessed by the fibrosis-4 index (FIB-4). Parametric proportional hazards models were used to estimate the adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs).
During a median follow-up of 4.0 years, 27 810 people with incident HS and 134 with incident HS plus high FIB-4 were identified. Compared with the non-depressed category, the aHR (95% CIs) for incident HS was 1.24 (1.15–1.34) for CES-D ⩾ 16 among obese individuals, and 1.00 (0.95–1.05) for CES-D ⩾ 16 among non-obese individuals (p for interaction with obesity <0.001). The aHR (95% CIs) for developing HS plus high FIB-4 was 3.41 (1.33–8.74) for CES-D ⩾ 16 among obese individuals, and 1.22 (0.60–2.47) for CES-D ⩾ 16 among non-obese individuals (p for interaction = 0.201).
Depression was associated with an increased risk of incident HS and HS plus high probability of advanced fibrosis, especially among obese individuals.
To detect early left ventricular dysfunction in children with non-alcoholic fatty liver disease using three-dimensional speckle tracking echocardiography.
Forty obese children with non-alcoholic fatty liver disease were included as group I. Another 40 obese children without non-alcoholic fatty liver disease of matched age, sex, and weight were included as group II. Forty healthy controls of matched age and sex served as a control group. Anthropometric measurements, laboratory investigations, and echocardiographic examinations including three-dimensional speckle tracking echocardiography were measured for all included children.
Abnormal lipid profile was detected in children with non-alcoholic fatty liver disease. Troponin I levels were significantly higher in children with non-alcoholic fatty liver disease compared to obese children without non-alcoholic fatty liver disease and to healthy controls. Three-dimensional speckle tracking echocardiography examination revealed a significant reduction of left ventricular global longitudinal strain, circumferential strain, radial strain, and area strain in children with non-alcoholic fatty liver disease inspite of normal left ventricular fraction shortening measured by conventional echocardiography. All strains were negatively correlated with the grade of non-alcoholic fatty liver disease.
Non-alcoholic fatty liver disease is associated with subclinical left ventricular dysfunction. Three-dimensional speckle tracking echocardiography can be helpful in identifying early left ventricular dysfunction in children with non-alcoholic fatty liver disease even in the presence of normal left ventricular ejection fraction.
The FNDC5 gene encodes the fibronectin type III domain-containing protein 5 that is a membrane protein mainly expressed in skeletal muscle, and the FNDC5 rs3480 polymorphism may be associated with liver disease severity in non-alcoholic fatty liver disease (NAFLD). We investigated the influence of the FNDC5 rs3480 polymorphism on the relationship between sarcopenia and the histological severity of NAFLD. A total of 370 adult individuals with biopsy-proven NAFLD were studied. The association between the key exposure sarcopenia and the outcome liver histological severity was investigated by binary logistic regression. Stratified analyses were undertaken to examine the impact of FNDC5 rs3480 polymorphism on the association between sarcopenia and the severity of NAFLD histology. Patients with sarcopenia had more severe histological grades of steatosis and a higher prevalence of significant fibrosis and definite non-alcoholic steatohepatitis than those without sarcopenia. There was a significant association between sarcopenia and significant fibrosis (adjusted OR 2·79, 95 % CI 1·31, 5·95, P = 0·008), independent of established risk factors and potential confounders. Among patients with sarcopenia, significant fibrosis occurred more frequently in the rs3480 AA genotype carriers than in those carrying the FNDC5 rs3480 G genotype (43·8 v. 17·2 %, P = 0·031). In the association between sarcopenia and liver fibrosis, there was a significant interaction between the FNDC5 genotype and sarcopenia status (P value for interaction = 0·006). Sarcopenia is independently associated with significant liver fibrosis, and the FNDC5 rs3480 G variant influences the association between sarcopenia and liver fibrosis in patients with biopsy-proven NAFLD.
The relationships between the total antioxidant capacity (TAC) of the diet and the risk of non-alcoholic fatty liver disease (NAFLD) have not previously been assessed. The aim of this study was to assess relationships between DTAC and odds of NAFLD in a case–control study. This case–control study was carried out in 158 patients with NAFLD and 357 healthy individuals aged 18–55 years. Dietary data were collected using validated 168-item quantitative food frequency questionnaires. Triacylglycerols (TAGs), total cholesterol (TC), high-density lipoprotein (HDL-C), low-density lipoprotein (LDL-C) and fasting blood glucose (FBS) concentrations were assessed using enzymatic methods and commercial kits. The DTAC was calculated based on the oxygen radical absorbance capacity of each food reported by the U.S. Department of Agriculture. The mean ± sd (standard deviation) for age and body mass index (BMI) of the study participants were 43⋅9 years ±5⋅9 and had 30⋅5 kg/m2 ±2⋅6. The NAFLD patients included higher BMI and female proportion, compared with the control group. The NAFLD patients included higher smoking rates, biochemical parameters (TG, TC, LDL-C and FBS) and DTAC scores, compared with control groups (P-value < 0⋅05). However, patients with NAFLD had lower HDL levels and physical activities, compared with the control group. The highest tertile of DTAC showed lower odds of NAFLD, compared with the lowest tertile. This association was significant after adjustment for potential confounders (OR, 0⋅19; 95 % CI, 0⋅9–0⋅34; P for trend 0⋅001). Findings suggest that the promotion of naturally increased antioxidant capacities may help prevent odds of NAFLD.
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Recent evidence has suggested the protective effects of honey consumption against the metabolic syndrome, but the association between honey intake and NAFLD is still unclear. We investigated how the consumption frequency of honey was associated with NAFLD in the general population. This was a cross-sectional study of 21 979 adults aged 20–90 years. NAFLD was diagnosed based on the ultrasound-diagnosed fatty liver without significant alcohol intake and other liver diseases. Diet information, including consumption frequency of honey, was assessed by a validated 100-item FFQ. OR with 95 % CI were calculated by the binary logistic regression model, adjusting for confounding factors identified by the directed acyclic graph. Overall, 6513 adults (29·6 %) had NAFLD. Compared with participants consuming ≤1 time/week of honey, the multivariable OR of NAFLD were 0·86 (95 % CI 0·77, 0·97) for 2–6 times/week and 1·10 (95 % CI 0·95, 1·27) for ≥1 times/d (Pfor trend = 0·90). The results were generally similar in subgroups of BMI at a cut-point of 24·0 kg/m2 (Pfor interaction = 0·10). In this large-scale study, consuming honey 2–6 times/week was inversely associated with NAFLD, whereas consuming honey ≥1 times/d had no association with NAFLD. These results need replication in other large-scale prospective studies.
Probiotics and plant extracts are considered to prevent the development of non-alcoholic fatty liver disease (NAFLD). The present study explores the effects of using both probiotics and plant extracts on NAFLD. The present study evaluated the effects of plant extracts on lipid droplet accumulation and the growth of probiotics in vitro. A C57BL/6 mouse model was used to examine the effects of probiotics and plant extracts on NAFLD. Body weight and food intake were measured. The levels of serum lipids, oxidative stress and the liver injury index were determined using commercial kits. Haematoxylin and eosin staining, GC and real-time PCR were also used for analysis. The results revealed that administration of Lactobacillus casei YRL577 and L. paracasei X11 with resveratrol (RES) or tea polyphenols (TP) significantly reduced the levels of total cholesterol, TAG and LDL-cholesterol and increased the level of the HDL-cholesterol. The groups of L. casei YRL577 with RES and TP also regulated the liver structure, oxidative stress and injury. Furthermore, L. casei YRL577 with TP exhibited a more positive effect towards improving the NAFLD and increased the concentrations of the butyric acid than other three combined groups. L. casei YRL577 with TP up-regulated the mRNA levels of the farnesoid X receptor and fibroblast growth factor 15 and decreased the mRNA levels of the apical Na-dependent bile acid transporter. These findings showed that L. casei YRL577 + TP-modified genes in the intestinal bile acid pathway improved markers of NAFLD.
Non-alcoholic fatty liver disease (NAFLD) has become the main cause of end-stage liver disease. Probiotics have the potential effect of alleviating NAFLD. The aim of this study was to explore functional probiotics and their underlying mechanisms. The bile salt hydrolase (BSH) activity in thirty-four strains was determined in vitro. Then, C57BL/6 mice were used to explore the effects of probiotics on NAFLD. Body weight and food intake were measured, and serum lipid concentrations, oxidative stress and proinflammatory cytokines levels were determined using commercial kits. The expressions of intestinal bile acid pathway genes were evaluated via real-time PCR. The results showed that Lactobacillus casei YRL577 and L. paracasei X11 had higher BSH activity. L. casei YRL577 significantly reduced liver weight and liver index and could regulate the levels of lipid metabolism, oxidative stress and proinflammatory cytokines as compared with L. paracasei X11. Furthermore, the results indicated that L. casei YRL577 up-regulated the mRNA levels of farnesoid X receptor and fibroblast growth factor 15, whereas down-regulated the mRNA level of apical Na-dependent bile acid transporter. These findings suggested that L. casei YRL577 modified genes in the intestinal bile acid pathway which might contribute to the alleviation of NAFLD.
Flavonoid-rich foods have shown a beneficial effect against non-alcoholic fatty liver disease (NAFLD) in short-term randomised trials. It is uncertain whether the usual dietary intake of flavonoids may benefit patients with NAFLD. The present study evaluated the association between the usual intake of flavonoids and the risk of progression in NAFLD. The prospective study included 2694 adults from the Guangzhou Nutrition and Health Study. Face-to-face interviews using a seventy-nine-item FFQ were administered to assess habitual dietary flavonoid intake, while abdominal ultrasonography was conducted to evaluate the presence and degree of NAFLD, with measurements conducted 3 years apart. After adjustment for potential confounders, higher flavonoid intakes were gradely associated with reduced risks of worsen NAFLD status. The relative risks of worsening (v. non-worsening) NAFLD in the highest (v. lowest) quintile were 0·71 (95 % CI 0·54, 0·93) for total flavonoids, 0·74 (95 % CI 0·57, 0·95) for flavanones, 0·74 (95 % CI 0·56, 0·96) for flavan-3-ols, 0·90 (95 % CI 0·68, 1·18) for flavonols, 0·73 (95 % CI 0·56, 0·93) for flavones, 0·79 (95 % CI 0·61, 1·02) for isoflavones and 0·74 (95 % CI 0·57, 0·96) for anthocyanins. An L-shaped relationship was observed between total flavonoid intake and the risk of NAFLD progression. Path analyses showed that the association between flavonoids and NAFLD progression was mediated by decreases in serum cholesterol and homeostasis model assessment of insulin resistance. This prospective study showed that higher flavonoid intake was associated with a lower risk of NAFLD progression in the elderly overweight/obese Chinese population.
Kefir consumption has been demonstrated to improve lipid and cholesterol metabolism; however, our previous study identified that benefits vary between different commercial and traditional kefir. Here, we investigate the ability of pitched culture kefir, that is, kefir produced by a small number of specific strains, to recapitulate health benefits of a traditional kefir, in a diet-induced obesity mouse model, and examine how microbial composition of kefir impacts these benefits. Eight-week-old female C57BL/6 mice were fed a high-fat diet (40 % energy from fat) supplemented with one of five kefir varieties (traditional, pitched, pitched with no Lactobacillus, pitched with no yeast and commercial control) at 2 ml in 20 g of food for 8 weeks prior to analysis of plasma and liver lipid profiles, and liver gene expression profiles related to lipid metabolism. Both traditional and pitched kefir lowered plasma cholesterol by about 35 % (P = 0·0005) and liver TAG by about 55 % (P = 0·0001) when compared with commercial kefir despite no difference in body weight. Furthermore, pitched kefir produced without either yeast or Lactobacillus did not lower cholesterol. The traditional and pitched kefir with the full complement of microbes were able to impart corresponding decreases in the expression of the cholesterol and lipid metabolism genes encoding 3-hydroxy-3-methylglutaryl-coenzyme A reductase, PPARγ and CD36 in the liver. These results demonstrate that traditional kefir organisms can successfully be utilised in a commercial process, while highlighting the importance of microbial interactions during fermentation in the ability of fermented foods to benefit host health.
A Nutrition Society member-led meeting was held on 9 January 2020 at The University of Surrey, UK. Sixty people registered for the event, and all were invited to participate, either through chairing a session, presenting a ‘3 min lightning talk’ or by presenting a poster. The meeting consisted of an introduction to the topic by Dr Barbara Fielding, with presentations from eight invited speakers. There were also eight lightning talks and a poster session. The meeting aimed to highlight recent research that has used stable isotope tracer techniques to understand human metabolism. Such studies have irrefutably shaped our current understanding of metabolism and yet remain a mystery to many. The meeting aimed to de-mystify their use in nutrition research.
Non-alcoholic fatty liver disease (NAFLD) includes a range of disorders from simple steatosis to non-alcoholic steatohepatitis. There is no proven drug treatment for NAFLD, and diet modification is considered part of the main line of treatment for this disease. The aim of this study was to investigate the efficacy of garlic supplementation in NAFLD patients. The effect of garlic powder supplementation on hepatic steatosis, liver enzymes and lipid profile was investigated in NAFLD patients. Ninety NAFLD patients were randomly assigned to take either a garlic powder supplement or a placebo for 12 weeks. The treatment group received four tablets of garlic daily (each tablet contained 400 mg garlic powder). The control group received four tablets of placebo (each placebo contained 400 mg starch). At the end of the study, hepatic steatosis was significantly reduced in the treatment group compared with the control group (P = 0·001). In addition, a significant decrease was seen in the serum concentration of alanine transaminase (P < 0·001), aspartate transaminase (P = 0·002), γ-glutamyltransferase (P = 0·003) as well as total cholesterol (P = 0·009), TAG (P < 0·001), HDL-cholesterol (P < 0·001) and LDL-cholesterol (P = 0·01) in the treatment group compared with the control group. No significant difference was seen between the two groups in serum concentration of alkaline phosphatase. Overall, garlic powder supplementation improved hepatic features and lipid profile among NAFLD patients.
To explore the association between dietary Na intake and non-alcoholic fatty liver disease (NAFLD) in a nationally representative sample of the US population.
In this cross-sectional study, the associations between Na intake and NAFLD, defined by the hepatic steatosis index (HSI) and the fatty liver index (FLI), were assessed through multivariable logistic regression models.
Communities in the USA from 2007 to 2014.
Men and women aged 20 years and older.
A total of 11 022 participants were included in the HSI-defined NAFLD analysis, and a subsample of 5320 participants was included in the FLI-defined NAFLD analysis. Compared with the lowest quartile of Na intake, the highest quartile had a multivariate-adjusted OR and 95 % CI of 1·46 (1·29, 1·65) for NAFLD as defined by HSI, and 1·41 (1·18, 1·69) for NAFLD as defined by FLI. This association was, to some degree, attenuated but remained significant after adjusting for several related metabolic parameters, including BMI, hypertension, hypercholesterolaemia, and diabetes.
Findings from the current study indicate that dietary Na intake is positively associated with NAFLD in US adults.