Dietary Fat Modulation of Gut Microbiota and Impact on Regulatory Pathways Controlling Food Intake.

Obesity is a multifactorial disease that continues to increase in prevalence worldwide. Emerging evidence has shown that the development of obesity may be influenced by taxonomic shifts in gut microbiota in response to the consumption of dietary fats. Further, these alterations in gut microbiota have been shown to promote important changes in satiation signals including gut hormones (leptin, ghrelin, GLP-1, peptide YY and CCK) and orexigenic and anorexigenic neuropeptides (AgRP, NPY, POMC, CART) that influence hyperphagia and therefore obesity. In this review, we highlight mechanisms by which gut microbiota can influence these satiation signals both locally in the gastrointestinal tract and via microbiota-gut-brain communication. Then, we describe the effects of dietary interventions and associated changes in gut microbiota on satiety signals through microbiota-dependent mechanisms. Lastly, we present microbiota optimizing therapies including prebiotics, probiotics, synbiotics and weight loss surgery that can help restore beneficial gut microbiota by enhancing satiety signals to reduce hyperphagia and subsequent obesity. Overall, a better understanding of the mechanisms by which dietary fats induce taxonomical shifts in gut microbiota and their impact on satiation signaling pathways will help develop more targeted therapeutic interventions in delaying the onset of obesity and in furthering its treatment.

Prediction of prolonged resolution of chylous ascites after radical D3 resection for colorectal cancer: A population-based experience from a high-volume center.

AIM: This study was aimed to analyze the incidence, risk factors, and management of chylous ascites (CA) after radical D3 resection for colorectal cancer, and to construct a predicting nomogram for prolonged resolution of CA. METHOD: Consecutive colorectal cancer patients who underwent radical D3 resection were included. Logistic analysis was used to identify risk factors of postoperative CA, as well as prolonged CA resolution. A predictive nomogram for prolonged resolution of CA was developed and validated internally. RESULTS: Among 7167 patients included, 277 (3.8%) patients developed CA. Logistic regression analysis demonstrated that laparoscopic operation (OR 1.507; P = 0.017) and tumors fed by the superior mesenteric artery (SMA, OR 2.456; P < 0.001) were independent risk factors of postoperative CA following radical D3 surgery for colorectal cancer. Open operation (OR 0.422; P = 0.027), drainage output on the first day of treatment (OR 1.004; P = 0.016), time to oral intake (OR 1.273; P = 0.042), and time to onset (OR 1.231; P = 0.024) were independently associated with prolonged resolution of postoperative CA (≥7 days). A predictive nomogram for prolonged CA resolution was developed with a C-index of 0.725. CONCLUSION: The incidence of CA after radical D3 surgery of colorectal cancer was 3.8%. Open operation, drainage output on the first day of treatment, time to oral intake, and time to onset were independently associated with prolonged resolution of postoperative CA. A nomogram may assist in tailored treatment decision-making and counseling patient with treatment strategies.

Insulin strategies for dietary fat and protein in type 1 diabetes: A systematic review.

AIM: To identify and report the efficacy of insulin strategies used to manage glycaemia following fat and/or fat and protein meals in type 1 diabetes. METHODS: A systematic literature search of medical databases from 1995 to 2021 was undertaken. Inclusion criteria were randomised controlled trials that reported at least one of the following glycaemic outcomes: mean glucose, area under the curve, time in range or hypoglycaemic episodes. RESULTS: Eighteen studies were included. Thirteen studies gave additional insulin. Five studies gave an additional 30%-43% of the insulin-to-carbohydrate ratio (ICR) for 32-50 g of fat and 31%-51% ICR for 7-35 g of fat with 12-27 g of protein added to control meals. A further eight studies gave -28% to +75% ICR using algorithms based on fat and protein for meals with 19-50 g of carbohydrate, 2-79 g of fat and 10-60 g of protein, only one study reported a glycaemic benefit of giving less than an additional 24% ICR. Eight studies evaluated insulin delivery patterns. Four of six studies in pump therapy, and one of two studies in multiple daily injections showed the combination of bolus and split dose, respectively, were superior. Five studies examined the insulin dose split, four demonstrated 60%-125% ICR upfront was necessary. Two studies investigated the timing of insulin delivery, both reported administration 15 min before the meal lowered postprandial glycaemia. CONCLUSIONS: Findings highlight the glycaemic benefit of an additional 24%-75% ICR for fat and fat and protein meals. For these meals, there is supportive evidence for insulin delivery in a combination bolus with a minimum upfront dose of 60% ICR, 15 min before the meal.

Effect of Enteral Lipid Supplement on Severe Retinopathy of Prematurity: A Randomized Clinical Trial.

Importance: Lack of arachidonic acid (AA) and docosahexaenoic acid (DHA) after extremely preterm birth may contribute to preterm morbidity, including retinopathy of prematurity (ROP). Objective: To determine whether enteral supplementation with fatty acids from birth to 40 weeks' postmenstrual age reduces ROP in extremely preterm infants. Design, Setting, and Participants: The Mega Donna Mega trial, a randomized clinical trial, was a multicenter study performed at 3 university hospitals in Sweden from December 15, 2016, to December 15, 2019. The screening pediatric ophthalmologists were masked to patient groupings. A total of 209 infants born at less than 28 weeks' gestation were tested for eligibility, and 206 infants were included. Efficacy analyses were performed on as-randomized groups on the intention-to-treat population and on the per-protocol population using as-treated groups. Statistical analyses were performed from February to April 2020. Interventions: Infants received either supplementation with an enteral oil providing AA (100 mg/kg/d) and DHA (50 mg/kg/d) (AA:DHA group) or no supplementation within 3 days after birth until 40 weeks' postmenstrual age. Main Outcomes and Measures: The primary outcome was severe ROP (stage 3 and/or type 1). The secondary outcomes were AA and DHA serum levels and rates of other complications of preterm birth. Results: A total of 101 infants (58 boys [57.4%]; mean [SD] gestational age, 25.5 [1.5] weeks) were included in the AA:DHA group, and 105 infants (59 boys [56.2%]; mean [SD] gestational age, 25.5 [1.4] weeks) were included in the control group. Treatment with AA and DHA reduced severe ROP compared with the standard of care (16 of 101 [15.8%] in the AA:DHA group vs 35 of 105 [33.3%] in the control group; adjusted relative risk, 0.50 [95% CI, 0.28-0.91]; P = .02). The AA:DHA group had significantly higher fractions of AA and DHA in serum phospholipids compared with controls (overall mean difference in AA:DHA group, 0.82 mol% [95% CI, 0.46-1.18 mol%]; P < .001; overall mean difference in control group, 0.13 mol% [95% CI, 0.01-0.24 mol%]; P = .03). There were no significant differences between the AA:DHA group and the control group in the rates of bronchopulmonary dysplasia (48 of 101 [47.5%] vs 48 of 105 [45.7%]) and of any grade of intraventricular hemorrhage (43 of 101 [42.6%] vs 42 of 105 [40.0%]). In the AA:DHA group and control group, respectively, sepsis occurred in 42 of 101 infants (41.6%) and 53 of 105 infants (50.5%), serious adverse events occurred in 26 of 101 infants (25.7%) and 26 of 105 infants (24.8%), and 16 of 101 infants (15.8%) and 13 of 106 infants (12.3%) died. Conclusions and Relevance: This study found that, compared with standard of care, enteral AA:DHA supplementation lowered the risk of severe ROP by 50% and showed overall higher serum levels of both AA and DHA. Enteral lipid supplementation with AA:DHA is a novel preventive strategy to decrease severe ROP in extremely preterm infants. Trial Registration: ClinicalTrials.gov Identifier: NCT03201588.

Dietary docosahexaenoic acid inhibits neurodegeneration and prevents stroke.

Stroke severely impairs quality of life and has a high mortality rate. On the other hand, dietary docosahexaenoic acid (DHA) prevents neuronal damage. In this review, we describe the effects of dietary DHA on ischemic stroke-associated neuronal damage and its role in stroke prevention. Recent epidemiological studies have been conducted to analyze stroke prevention through DHA intake. The effects of dietary intake and supply of DHA to neuronal cells, DHA-mediated inhibition of neuronal damage, and its mechanism, including the effects of the DHA metabolite, neuroprotectin D1 (NPD1), were investigated. These studies revealed that DHA intake was associated with a reduced risk of stroke. Moreover, studies have shown that DHA intake may reduce stroke mortality rates. DHA, which is abundant in fish oil, passes through the blood-brain barrier to accumulate as a constituent of phospholipids in the cell membranes of neuronal cells and astrocytes. Astrocytes supply DHA to neuronal cells, and neuronal DHA, in turn, activates Akt and Raf-1 to prevent neuronal death or damage. Therefore, DHA indirectly prevents neuronal damage. Furthermore, NDP1 blocks neuronal apoptosis. DHA, together with NPD1, may block neuronal damage and prevent stroke. The inhibitory effect on neuronal damage is achieved through the antioxidant (via inducing the Nrf2/HO-1 system) and anti-inflammatory effects (via promoting JNK/AP-1 signaling) of DHA.

Effect of lipid-based nutrient supplement-Medium quantity on reduction of stunting in children 6-23 months of age in Sindh, Pakistan: A cluster randomized controlled trial.

BACKGROUND: Chronic childhood malnutrition, or stunting, remains a persistent barrier to achieve optimal cognitive development, child growth and ability to reach full potential. Almost half of children under-five years of age are stunted in the province of Sindh, Pakistan. OBJECTIVE: The primary objective of this study was to test the hypothesis that the provision of lipid-based nutrient supplement-medium-quantity (LNS-MQ) known as Wawamum will result in a 10% reduction in risk of being stunted at the age of 24 months in the intervention group compared with the control group. DESIGN: A cluster randomized controlled trial was conducted in Thatta and Sujawal districts of Sindh province, Pakistan. A total of 870 (419 in intervention; 451 in control) children between 6-18 months old were enrolled in the study. The unit of randomization was union council and considered as a cluster. A total of 12 clusters, 6 in each study group were randomly assigned to intervention and control group. All children received standard government health services, while children in the intervention group also received 50 grams/day of Wawamum. RESULTS: Children who received Wawamum were found to have a significantly reduced risk of stunting (RR = 0.91, 95% CI; 0.88-0.94, p<0.001) and wasting (RR = 0.78, 95% CI; 0.67-0.92, p = 0.004) as compared to children who received the standard government health services. There was no evidence of a reduction in the risk of underweight (RR = 0.94, 95% CI; 0.85-1.04, p = 0.235) in the intervention group compared to the control group. Statistically significant reduction in anaemia in the intervention group was also found as compared to the control group (RR = 0.97, 95% CI; 0.94-0.99, p = 0.042). The subgroup analysis by age, showed intervention effect is significant in reduction of risk of stunting in younger children of aged 6-12 month (RR = 0.83, 95% CI; 0.81-0.86, p = <0.001) and their older peers aged 13-18 month- (RR = 0.90, 95% CI; 0.83-0.97, p = 0.008). The mean compliance of Wawamum was 60% among children. CONCLUSIONS: The study confirmed that the provision of Wawamum to children 6-23 months of age is effective in reducing the risk of stunting, wasting and anaemia. This approach should be scaled up among the most food insecure areas/households with a high prevalence of stunting to achieve positive outcomes for nutrition and health. This study was registered at clinicaltrials.gov as NCT02422953. Clinical Trial Registration Number: NCT02422953.

Gastrointestinal Disorders and Metabolic Syndrome: Dysbiosis as a Key Link and Common Bioactive Dietary Components Useful for their Treatment.

Gastrointestinal (GI) diseases, which include gastrointestinal reflux disease, gastric ulceration, inflammatory bowel disease, and other functional GI disorders, have become prevalent in a large part of the world population. Metabolic syndrome (MS) is cluster of disorders including obesity, hyperglycemia, hyperlipidemia, and hypertension, and is associated with high rate of morbidity and mortality. Gut dysbiosis is one of the contributing factors to the pathogenesis of both GI disorder and MS, and restoration of normal flora can provide a potential protective approach in both these conditions. Bioactive dietary components are known to play a significant role in the maintenance of health and wellness, as they have the potential to modify risk factors for a large number of serious disorders. Different classes of functional dietary components, such as dietary fibers, probiotics, prebiotics, polyunsaturated fatty acids, polyphenols, and spices, possess positive impacts on human health and can be useful as alternative treatments for GI disorders and metabolic dysregulation, as they can modify the risk factors associated with these pathologies. Their regular intake in sufficient amounts also aids in the restoration of normal intestinal flora, resulting in positive regulation of insulin signaling, metabolic pathways and immune responses, and reduction of low-grade chronic inflammation. This review is designed to focus on the health benefits of bioactive dietary components, with the aim of preventing the development or halting the progression of GI disorders and MS through an improvement of the most important risk factors including gut dysbiosis.

Effect of two different dietary fatty acid profiles and variant rs266729 in ADIPOQ on weight loss and adiponectin concentrations / Efecto de dos perfiles diferentes de ácidos grasos en la dieta y variante en el gen rs266729 de adiponectina sobre la pérdida de peso y los niveles de adiponectina

BACKGROUND: The role of ADIPOQ gene rs266729 variants on weight loss after a dietary intervention are still unclear. OBJECTIVE: To analyze the effects of the ADIPOQ gene rs266729 variant n weight loss, cardiovascular risk factors, and adiponectin levels after two hypocaloric diets with different dietary fatty profiles. DESIGN: A population of 362 obese patients was enrolled in a randomized clinical trial with two diets (Diet M, monounsaturated fat-enriched diet, and Diet P, polyunsaturated-fat enriched diet). Anthropometric measurements, an assessment of nutritional intake, and biochemical tests were performed at baseline and after 12 weeks. RESULTS: Weight loss was similar with both diets. After Diet M, only subjects with CC genotype showed significant improvements in total cholesterol (CC vs. CG ± GG) -9.0 ±1.1 mU/L vs. -4.5 ± 2.4 mg/dL, p = 0.01), LDL cholesterol (-6.0 ± 1.1 mg/dL vs. -3.0 ± 0.9 mg/dL, p = 0.03), glucose (-4.7 ± 1.1 mg/dL vs. -0.6 ± 0.5 mg/dL, p = 0.01), and insulin levels (-2.6 ±1.0 mU/L vs. -0.7 ± 0.3 mU/L, p = 0.02) and in HOMA-IR (-0.5 ± 0.2 units vs. -0.2 ± 0.4 units, p = 0.03). The same improvement was reported after Diet P in all parameters, including total cholesterol (CC vs. CG±GG) (-8.0 ± 1.2mU/L vs. -2.1 ± 1.4 mg/dL, p = 0.02), LDL cholesterol (-7.3 ± 1.2 mg/dL vs. -2.1 ± 0.8 mg/dL, p = 0.02), glucose (-3.2 ± 0.1mg/dL vs. -0.2 ± 0.5 mg/dL, p = 0.01), and insulin levels (-2.5 ± 1.0 mU/L vs. -1 ± 0.6 mU/L, p = 0.02) and HOMA-IR (-0.5 ± 0.1 units vs. −0.3 ± 0.4 units, p = 0.02). Only subjects with CC genotype showed significant increases in adiponectin levels after both diets: (Diet M: 10.3 ± 2.0 ng/dL vs. Diet P: 9.3 ± 2.9 ng/dL, p = 0.43). CONCLUSION: The CC genotype of ADIPOQ gene rs266729 variant is associated to increased adiponectin levels and decreases in LDL cholesterol, glucose, insulin, and HOMA-IR levels after weight loss

ANTECEDENTES: El papel de las variantes del gen ADIPOQ en la pérdida de peso después de una intervención dietética sigue sin estar claro. OBJETIVO: Nuestro objetivo fue analizar los efectos de la variante rs266729 del gen ADIPOQ sobre la pérdida de peso, los factores de riesgo cardiovascular y los niveles de adiponectina después de 2 dietas hipocalóricas con diferentes perfiles de grasas en la dieta. DISEÑO: Una población de 362 pacientes obesos se incluyeron en un ensayo clínico aleatorizado con 2 dietas (dieta M: dieta enriquecida con grasas monoinsaturadas y dieta P: dieta enriquecida con grasas poliinsaturadas). Antes y tras 12 semanas, se realizó una evaluación antropométrica, evaluación de la ingesta nutricional y un análisis bioquímico. RESULTADOS: La pérdida de peso fue similar con ambas dietas. Después de la dieta M, solo los sujetos con genotipo CC mostraron una mejoría significativa en el colesterol total (CC vs. CG±GG) (-9,0 ± 1,1 mU/l vs. - 4,5 ± 2,4 mg/dl; p = 0,01), colesterol LDL (-6,0 ± 1,1 mg/dl vs. - 3,0 ± 0,9 mg/dl; p = 0,03), glucosa (-4,7 ± 1,1 mg/dl vs. -0,6 ± 0,5 mg/dl; p = 0,01), niveles de insulina (-2,6 ± 1,0 mU/l vs. -0,7± 0,3 mU/l; p = 0,02) y HOMA-IR (- 0,5 ± 0,2 unidades vs. -0,2 ± 0,4 unidades; p = 0,03). La misma mejora en todos los parámetros se informó después de la dieta P; niveles de colesterol total (CC vs. CG ± GG) (-8,0 ± 1,2 mU/l vs. -2,1 ± 1,4 mg/dl; p = 0,02), colesterol LDL (-7,3 ± 1,2 mg/dl vs. -2,1 ±0,8 mg/dl; p = 0,02), glucosa (-3,2 ± 0,1 mg/dl vs. -0,2 ± 0,5 mg/dl; p = 0,01), niveles de insulina (-2,5 ±1,0 mU/l vs. -1 ±0,6 mU/l; p = 0,02) y HOMA-IR (-0,5 ± 0,1 unidades vs. -0,3 ± 0,4 unidades; p = 0,02). Solo los sujetos con genotipo CC mostraron un aumento significativo de los niveles de adiponectina después de ambas dietas: (dieta M: 10,3 ± 2,0 ng/dl vs. dieta P: 9,3 ± 2,9 ng/dl; p = 0,43). CONCLUSIÓN: El genotipo CC de la variante rs266729 del gen ADIPOQ se asocia con aumentos en los niveles de adiponectina y disminución del colesterol LDL, glucosa, insulina y HOMA-IR tras la pérdida de peso

The Effect of Coconut Oil Consumption on Cardiovascular Risk Factors: A Systematic Review and Meta-Analysis of Clinical Trials.

BACKGROUND: Coconut oil is high in saturated fat and may, therefore, raise serum cholesterol concentrations, but beneficial effects on other cardiovascular risk factors have also been suggested. Therefore, we conducted a systematic review of the effect of coconut oil consumption on blood lipids and other cardiovascular risk factors compared with other cooking oils using data from clinical trials. METHODS: We searched PubMed, SCOPUS, Cochrane Registry, and Web of Science through June 2019. We selected trials that compared the effects of coconut oil consumption with other fats that lasted at least 2 weeks. Two reviewers independently screened articles, extracted data, and assessed the study quality according to the PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). The main outcomes included low-density lipoprotein cholesterol (LDL-cholesterol), high-density lipoprotein cholesterol (HDL-cholesterol), total cholesterol, triglycerides, measures of body fatness, markers of inflammation, and glycemia. Data were pooled using random-effects meta-analysis. RESULTS: 16 articles were included in the meta-analysis. Results were available from all trials on blood lipids, 8 trials on body weight, 5 trials on percentage body fat, 4 trials on waist circumference, 4 trials on fasting plasma glucose, and 5 trials on C-reactive protein. Coconut oil consumption significantly increased LDL-cholesterol by 10.47 mg/dL (95% CI: 3.01, 17.94; I2 = 84%, N=16) and HDL-cholesterol by 4.00 mg/dL (95% CI: 2.26, 5.73; I2 = 72%, N=16) as compared with nontropical vegetable oils. These effects remained significant after excluding nonrandomized trials, or trials of poor quality (Jadad score <3). Coconut oil consumption did not significantly affect markers of glycemia, inflammation, and adiposity as compared with nontropical vegetable oils. CONCLUSIONS: Coconut oil consumption results in significantly higher LDL-cholesterol than nontropical vegetable oils. This should inform choices about coconut oil consumption.

Efecto del polimorfismo rs10830963 MTNR1B y la composición de grasa de la dieta en la resistencia a la insulina tras la pérdida de peso durante 3 meses / Dietary-fat effect of the rs10830963 polymorphism in MTNR1B on insulin resistance in response to 3 months weight-loss diets

ANTECEDENTES Y OBJETIVOS: El alelo de riesgo (G) de la variante rs10830963 en el gen del receptor de melatonina 1 B (MTNR1B) se relaciona con la obesidad. En este trabajo evaluamos el efecto de este SNP sobre los factores de riesgo cardiovascular y la pérdida de peso secundaria a 2 dietas hipocalóricas. MÉTODOS: Trescientos sesenta y un sujetos obesos fueron asignados aleatoriamente durante 3 meses (dieta M: dieta hipocalórica alta en grasas monoinsaturadas vs. dieta P: dieta hipocalórica alta en grasas poliinsaturadas). Se midieron los parámetros antropométricos, glucemia en ayunas, proteína C reactiva, concentración de insulina, resistencia a la insulina (HOMA-IR), perfil de lípidos y los niveles de adipocitoquinas. Se evaluó el genotipo del polimorfismo del gen MTNR1B (rs10830963). RESULTADOS: Todos los parámetros antropométricos, la presión arterial sistólica y los niveles de leptina disminuyeron en todos los sujetos después de ambas dietas. Esta mejora de los parámetros antropométricos fue mayor en los no portadores del alelo G que en los portadores del alelo G. Tras la intervención con dieta M (CC vs. CG + GG), el colesterol total (delta: -10,4 ± 2,1 mg/dl vs. -6,4 ± 1,2 mg/dl: p < 0,05), colesterol LDL (delta: -7,1 ± 0,9 mg/dl vs. -2,8 ± 0,8 mg/dl: p < 0,05), insulina (delta: -3,0 ± 0.8 UI/l vs. -2,0 ± 1,0 UI/l: p < 0,05) y HOMA IR (delta: -3,4 ± 1,0 unidades vs. -2,9 ± 0,9 unidades: p < 0,05) mejoraron en los no portadores del alelo G. Tras la dieta P, en el grupo de sujetos sin alelo G, los niveles de insulina (delta: -2,9 ± 1,0 UI/l vs. -0,6 ± 0,2 UI/l: p < 0,05) y HOMA-IR (delta [CC vs. CG + GG]: -0,8 ± 0,2 unidades vs. -0,4 ± 0,3 unidades: p < 0,05) también disminuyeron. CONCLUSIONES: Nuestro estudio detectó una relación de la variante rs10830963 de MTNR1B con la pérdida de peso corporal y la modificación de la resistencia a la insulina inducida por 2 dietas hipocalóricas diferentes. Solo la dieta hipocalórica enriquecida en grasa monoinsaturada y los no portadores del alelo G mostraron un efecto significativo sobre las lipoproteínas

BACKGROUND & AIMS: The risk allele (G) of rs10830963 in the melatonin receptor 1 B (MTNR1B) gene presents an association with obesity. We study the effect of this SNP on cardiovascular risk factors and weight loss secondary to 2hypocaloric diets. Methods: 361 obese subjects were randomly allocated during 3 months (Diet M - high monounsaturated fat hypocaloric diet vs. Diet P - high polyunsaturated fat hypocaloric diet). Anthropometric parameters, fasting blood glucose, C-reactive protein (CRP), insulin concentration, insulin resistance (HOMA-IR), lipid profile and adipocytokines levels were measured. Genotype of MTNR1B gene polymorphism (rs10830963) was evaluated. Results: All anthropometric parameters, systolic blood pressure and leptin levels decreased in all subjects after both diets. This improvement of anthropometric parameters was higher in non G allele carriers than G allele carriers. After dietary intervention with Diet M, (CC vs. CG + GG); total cholesterol (delta: -10.4 ± 2.1 mg/dl vs. -6.4 ± 1.2 mg/dl: P <.05), LDL-cholesterol (delta:-7.1 ± 0.9 mg/dl vs. -2.8 ± 0.8 mg/dl: P <.05), insulin (delta:-3.0 ± 0.8 UI/L vs. -2.0 ± 1.0 UI/L: P<.05) and HOMA-IR (delta:-3.4 ± 1.0 units vs. -2.9 ± 0.9 units: P<.05) improved in no G allele carriers. After Diet P, in the group of subjects without G allele CC, insulin levels (delta: -2.9 ± 1.0 UI/L vs. -0.6 ± 0.2 UI/L: P <.05) and HOMA-IR (delta (CC vs. CG + GG): -0.8 ± 0.2 units vs. -0.4 ± 0.3 units: P <.05) decreased, too. Conclusions: Our study detected a relationship of rs10830963 MTNR1B SNP with body weight loss and insulin resistance modification induced by 2 different hypocaloric. Only monounsaturated enriched hypocaloric diet and in no-G allele carriers showed a significant effect on lipoproteins

The Impact of Dairy Products in the Development of Type 2 Diabetes: Where Does the Evidence Stand in 2019?

The prevalence of type 2 diabetes (T2D) has increased rapidly. Adopting a heathy diet is suggested as one of the effective behaviors to prevent or delay onset of T2D. Dairy consumption has been recommended as part of a healthy diet, but there remains uncertainty in both the scientific community and the public about the effect of different dairy products on T2D risk. In a recent workshop, the evidence on dairy products and T2D risk was presented and discussed by a group of experts. The main conclusions from the workshop are presented in this position paper and are as follows. 1) Available evidence from large prospective cohort studies and limited randomized controlled trials (RCTs) suggests that total dairy consumption has a neutral or moderately beneficial effect on T2D risk. 2) Increasing evidence from prospective cohort studies indicates that yogurt is most strongly associated with a lower T2D risk, but evidence from RCTs is scarce. 3) Fatty acids from dairy (medium-chain, odd, and very long-chain SFAs as well as trans-palmitoleic acid) are associated with lower T2D risk and improved metabolic health, but more research is needed on studies that explore cause and effect relations to exclude the possibility that the dairy fatty acids simply serve as markers of overall dairy consumption. 4) The food matrix can be a stronger determinant of health effects than SFA content. This review further identifies research gaps in the existing knowledge and highlights key research questions that need to be addressed to better understand the impact of dairy consumption on future T2D risk.

[Primary intestinal lymphangiectasia: first case report in Peru]. / Linfangiectasia intestinal primaria: primer reporte de caso en Perú.

Primary intestinal lymphangiectasia is a rare clinical condition of unknown etiology. The common age of presentation is during the first 3 years of life, but cases in adults have also been reported. It has a variable symptomatology, but the main clinical manifestation is edema, also diarrhea and weight loss can occur. The loss of lymph fluid into the gastrointestinal tract also leads to hypoproteinemia and lymphopenia. Diagnosis is based on clinical manifestations, laboratory and endoscopic findings, and is confirmed on histopathological examination of biopsy. The main treatment is a protein rich, low in fat and medium chain triglyceride diet. We present the case of a 1-year-old male patient who presents with generalized edema, predominantly in lower limbs, and diarrhea. Laboratory findings show the presence of marked hypoproteinemia. Then an endoscopy and a duodenal biopsy are performed, and the histopathological study confirms the diagnosis of primary intestinal lymphangiectasia. The patient is treated and after a satisfactory evolution, is discharged.

Potential Nutritional and Metabolomic Advantages of High Fat Oral Supplementation in Pancreatectomized Pancreaticobiliary Cancer Patients.

We examined the effect of high fat oral nutritional supplement (HFS) on the nutritional status, oral intake, and serum metabolites of postoperative pancreaticobiliary cancer patients. Pancreaticobiliary cancer patients were voluntarily recruited. The HFS group received postoperative oral high fat supplementation (80% of total calories from fat; n = 12) until discharge; the control group (non-HFS; n = 9) received none. Dietary intake, anthropometry, blood chemistry, nutritional risk index (NRI), and serum metabolites analyzed by liquid chromatography tandem mass spectrometry were evaluated. Overall, cumulative caloric supply via parental and oral/enteral routes were not different between groups. However, oral fat intake, caloric intake, and NRI scores of the HFS group were higher than those of the non-HFS group with increased oral meal consumption. Oral caloric, fat, and meal intakes correlated with NRI scores. Metabolomics analysis identified 195 serum metabolites pre-discharge. Oral fat intake was correlated with 42 metabolites relevant to the glycerophospholipid pathway. Oral high fat-specific upregulation of sphingomyelin (d18:1/24:1), a previously reported pancreatic cancer-downregulated metabolite, and lysophosphatidylcholine (16:0) were associated with NRI scores. Provision of HFS in postoperative pancreatic cancer patients may facilitate the recovery of postoperative health status by increasing oral meal intake, improving nutritional status, and modulating serum metabolites.

What's new in atopic eczema? An analysis of systematic reviews published in 2016. Part 1: treatment and prevention.

This review is part of a series of annual updates summarizing the evidence base for atopic eczema (AE). It provides a summary of key findings from 28 systematic reviews that were published or indexed during 2016 with a focus on treatment and prevention of AE. There is reasonable evidence of benefit for topical corticosteroids, calcineurin inhibitors, a glycyrrhetinic acid-containing preparation (Atopiclair® ), oral ciclosporin, oral azathioprine, narrowband ultraviolet B radiation and education programmes. Overall, there is evidence that topical corticosteroids and calcineurin inhibitors have similar efficacy and that both can prevent AE flares when used twice weekly as maintenance therapy. However, topical calcineurin inhibitors are costlier and have more adverse reactions, thus topical corticosteroids should remain the standard of care for patients with AE. There is no evidence that multiple applications are better than once-daily application of topical corticosteroid. There is inconsistent evidence to support omalizumab and specific allergen immunotherapy use in AE. There is some evidence that vitamin D supplementation and synbiotics reduce AE severity, although the margin of improvement may not be clinically meaningful. There is little evidence to support the use of wet wraps or of complementary/alternative medicine (including Chinese herbal medicine). There is some evidence to suggest that a diet high in fish in infancy may be preventative for AE, but other dietary interventions for the prevention of AE show little promise. This review provides a succinct guide for clinicians and patients wishing to remain up to date with the latest evidence for the treatment and prevention of AE.

Marine n-3 Polyunsaturated Fatty Acids and the Risk of Ischemic Stroke.

Background and Purpose- We hypothesized that total marine n-3 polyunsaturated fatty acids (PUFA), in particular eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the diet and in adipose tissue (biomarkers of long-term intake and endogenous exposure) were inversely associated with the risk of ischemic stroke and its subtypes. Methods- The Diet, Cancer and Health cohort consisted of 57 053 participants aged 50 to 65 years at enrolment. All participants filled in a food frequency questionnaire and had an adipose tissue biopsy taken at baseline. Information on ischemic stroke during follow-up was obtained from The Danish National Patient Register, and all cases were validated. Cases and a random sample of 3203 subjects from the whole cohort had their fatty acid composition of adipose tissue determined by gas chromatography. Results- During 13.5 years of follow-up 1879 participants developed an ischemic stroke. Adipose tissue content of EPA was inversely associated with total ischemic stroke (hazard ratio [HR], 0.74; 95% CI, 0.62-0.88) when comparing the highest with the lowest quartile. Also, lower rates of large artery atherosclerosis were seen with higher intakes of total marine n-3 PUFA (HR, 0.69; 95% CI, 0.50-0.95), EPA (HR, 0.66; 95% CI, 0.48-0.91) and DHA (HR, 0.72; 95% CI, 0.53-0.99), and higher adipose tissue content of EPA (HR, 0.52; 95% CI, 0.36-0.76). Higher rates of cardioembolism were seen with higher intakes of total marine n-3 PUFA (HR, 2.50; 95% CI, 1.38-4.53) and DHA (HR, 2.12; 95% CI, 1.21-3.69) as well as with higher adipose tissue content of total marine n-3 PUFA (HR, 2.63; 95% CI, 1.33-5.19) and DHA (HR, 2.00; 95% CI, 1.04-3.84). The EPA content in adipose tissue was inversely associated with small-vessel occlusion (HR, 0.69; 95% CI, 0.55-0.88). Conclusions- EPA was associated with lower risks of most types of ischemic stroke, apart from cardioembolism, while inconsistent findings were observed for total marine n-3 PUFA and DHA.

Omega-3 fatty acid supplementation attenuates skeletal muscle disuse atrophy during two weeks of unilateral leg immobilization in healthy young women.

Omega-3 (n-3) fatty acid supplementation enhances muscle protein synthesis and muscle size. Whether n-3 fatty acid supplementation attenuates human muscle disuse atrophy is unknown. We determined the influence of n-3 fatty acid supplementation on muscle size, mass, and integrated rates of myofibrillar protein synthesis (MyoPS) following 2 wk of muscle disuse and recovery in women. Twenty women (BMI = 23.0 ± 2.3 kg/m2, age = 22 ± 3 yr) underwent 2 wk of unilateral limb immobilization followed by 2 wk of return to normal activity. Starting 4 wk prior to immobilization, participants consumed either 5 g/d of n-3 fatty acid or an isoenergetic quantity of sunflower oil (control). Muscle size and mass were measured pre- and postimmobilization, and after recovery. Serial muscle biopsies were obtained to measure integrated (daily) MyoPS. Following immobilization, the decline in muscle volume was greater in the control group compared to the n-3 fatty acid group (14 vs. 8%, P < 0.05) and was not different from preimmobilization at recovery in the n-3 fatty acid group; however, it was still lower in the control group ( P < 0.05). Muscle mass was reduced in the control group only ( P < 0.05). MyoPS was higher in the n-3 group compared with the control group at all times ( P < 0.05). We conclude that n-3 fatty acid supplementation attenuates skeletal muscle disuse atrophy in young women, which may be mediated by higher rates of MyoPS.-McGlory, C., Gorissen, S. H. M., Kamal, M., Bahniwal, R., Hector, A. J., Baker, S. K., Chabowski, A., Phillips, S. M. Omega-3 fatty acid supplementation attenuates skeletal muscle disuse atrophy during two weeks of unilateral leg immobilization in healthy young women.

Linfangiectasia intestinal primaria: primer reporte de caso en Perú / Primary intestinal lymphangiectasia: first case report in Peru

La linfangiectasia intestinal primaria es una entidad clínica poco común de etiología desconocida. La edad típica de presentación de esta enfermedad es durante los 3 primeros años de vida, pero también se han reportado casos en adultos. Posee sintomatología variable, pero la manifestación clínica principal es el edema, puede presentarse también diarrea y pérdida de peso. La pérdida de fluido linfático en el tracto gastointestinal conlleva también a hipoproteinemia y linfopenia. El diagnóstico se establece en base a la clínica, a los estudios de laboratorio, al estudio endoscópico y se confirma con la evaluación histológica de la biopsia realizada. El manejo se da mediante una dieta rica en proteínas, baja en grasas y triglicéridos de cadena media. A continuación, se presenta el caso de un paciente varón de 1 año de edad que presenta edema generalizado, con predominio de miembros inferiores, y diarrea. Los exámenes de laboratorio muestran la presencia de hipoproteinemia marcada. Posteriormente, se realiza una endoscopía digestiva alta y una biopsia duodenal. El estudio histológico confirma el diagnóstico de linfangiectasia intestinal primaria. El paciente recibe el tratamiento establecido para esta enfermedad y, finalmente es dado de alta.

Primary intestinal lymphangiectasia is a rare clinical condition of unknown etiology. The common age of presentation is during the first 3 years of life, but cases in adults have also been reported. It has a variable symptomatology, but the main clinical manifestation is edema, also diarrhea and weight loss can occur. The loss of lymph fluid into the gastrointestinal tract also leads to hypoproteinemia and lymphopenia. Diagnosis is based on clinical manifestations, laboratory and endoscopic findings, and is confirmed on histopathological examination of biopsy. The main treatment is a protein rich, low in fat and medium chain triglyceride diet. We present the case of a 1-year-old male patient who presents with generalized edema, predominantly in lower limbs, and diarrhea. Laboratory findings show the presence of marked hypoproteinemia. Then an endoscopy and a duodenal biopsy are performed, and the histopathological study confirms the diagnosis of primary intestinal lymphangiectasia. The patient is treated and after a satisfactory evolution, is discharged.

Dietary lipids with potential to affect satiety: Mechanisms and evidence.

Dietary fat has been implicated in the rise of obesity due to its energy density, palatability and weak effects on satiety. As fat is a major contributor to overall energy intake, incorporating fat with satiating properties could potentially reduce energy intake. This review outlines the potential mechanisms, as far as we know, by which Medium-Chain Triglycerides (MCT), Conjugated Linoleic Acid (CLA), Short-Chain Fatty Acids (SCFA), Diacylglycerol (DAG), n-3 PUFA, and Small Particle Lipids, exerts their satiating effects. The evidence suggests that the lipid with the most potential to enhance satiety is MCT. SCFA can also promote satiety, but oral administration has been linked to poor tolerability rather than satiety. Data on the appetite effects of CLA is limited but does suggest potential. Research comparing these lipids to each other is also lacking and should be explored to elucidate which of these 'functional lipids' is the most beneficial in enhancing satiety.

Olive oil lessened fatty liver severity independent of cardiometabolic correction in patients with non-alcoholic fatty liver disease: A randomized clinical trial.

OBJECTIVES: Olive oil has health benefits for the correction of metabolic diseases. We aimed to evaluate the effect of olive oil consumption on the severity of fatty liver and cardiometabolic markers in patients with non-alcoholic fatty liver disease. METHODS: This randomized, double-blind, clinical trial was conducted on 66 patients with non-alcoholic fatty liver disease. Patients were divided to receive either olive or sunflower oil, each 20 g/d for 12 wk. A hypocaloric diet (-500 kcal/d) was recommended to all participants. Fatty liver grade, liver enzymes, anthropometric parameters, blood pressure, serum lipid profile, glucose, insulin, malondialdehyde, total antioxidant capacity, and interleukin-6 were assessed pre- and postintervention. RESULTS: Fatty liver grade, weight, waist circumference, and blood pressure significantly decreased in both groups. Sunflower oil significantly reduced serum aspartate and alanine aminotransferases and olive oil only decreased serum aspartate aminotransferase. Fat-free mass and skeletal muscle mass significantly reduced after the consumption of sunflower oil and serum triacylglycerols and fat mass significantly declined after the ingestion of olive oil. Among these variables, only changes in fatty liver grade (-0.29 ± 0.46 in sunflower oil versus -0.75 ± 0.45 in olive oil; P < 0.001), skeletal muscle mass (-0.71 ± 1.36 in sunflower oil versus +0.45 ± 2.8 in olive oil; P = 0.04), and body fat percentage (+0.38 ± 5.2% in sunflower oil versus -3.4 ± 5.5% in olive oil; P = 0.04) were significantly different between the groups. CONCLUSIONS: Olive oil may alleviate the severity of fatty liver independent of correcting cardiometabolic risk factors. Low-calorie diets may benefit patients with non-alcoholic fatty liver disease additionally through mitigation of obesity, blood pressure, and liver enzymes.

Corn Oil Lowers Plasma Cholesterol Compared with Coconut Oil in Adults with Above-Desirable Levels of Cholesterol in a Randomized Crossover Trial.

Background: Few trials have examined the effects of coconut oil consumption in comparison with polyunsaturated fatty acid-rich oils such as corn oil. Objective: This trial assessed the effects of consuming foods made with corn oil compared with coconut oil on lipids, glucose homeostasis, and inflammation. Methods: This was a preliminary randomized crossover study of men (n = 12) and women (n = 13) with a mean age of 45.2 y, mean body mass index (in kg/m2) of 27.7, fasting LDL cholesterol ≥115 mg/dL and <190 mg/dL, and triglycerides (TGs) ≤375 mg/dL. Subjects consumed muffins and rolls providing 4 tablespoons (∼54 g) per day of corn oil or coconut oil as part of their habitual diets for 4 wk, with a 3-wk washout between conditions. Fasting plasma lipids and high-sensitivity C-reactive protein (hs-CRP) and glucose metabolism were assessed via an intravenous glucose tolerance test at baseline and 15 and 29 d of treatment. Responses were compared between treatments by ANCOVA. Results: Median baseline concentrations of LDL cholesterol, non-HDL cholesterol, total cholesterol (total-C), HDL cholesterol, total-C:HDL cholesterol, and TGs were 123, 144, 188, 46.0, 4.21, and 92.5 mg/dL, respectively. Changes from baseline for corn oil and coconut oil conditions, respectively, were: LDL cholesterol (primary outcome; -2.7% compared with +4.6%), non-HDL cholesterol (-3.0% compared with +5.8%), total-C (-0.5% compared with +7.1%), HDL cholesterol (+5.4% compared with +6.5%), total-C:HDL cholesterol (-4.3% compared with -3.3%), and TGs (-2.1% compared with +6.0%). Non-HDL cholesterol responses were significantly different between corn and coconut oil conditions (P = 0.034); differences between conditions in total-C and LDL cholesterol approached significance (both P = 0.06). Responses for hs-CRP and carbohydrate homeostasis parameters did not differ significantly between diet conditions. Conclusions: When incorporated into the habitual diet, consumption of foods providing ∼54 g of corn oil/d produced a more favorable plasma lipid profile than did coconut oil in adults with elevated cholesterol. This trial was registered at clinicaltrials.gov as NCT03202654.