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Metabolic health across the BMI spectrum in HIV-infected and HIV-uninfected men.
Lake, JE, Li, X, Palella, FJ, Erlandson, KM, Wiley, D, Kingsley, L, Jacobson, LP, Brown, TT
AIDS (London, England). 2018;(1):49-57
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Abstract
OBJECTIVES In the general population, metabolic health often declines as BMI increases. However, some obese individuals maintain metabolic health. HIV and antiretroviral therapy have been associated with metabolic disturbances. We hypothesized that HIV-infected (HIV) men on suppressive antiretroviral therapy experience less metabolic health than HIV-uninfected (HIV) men across all BMI categories. DESIGN/METHODS In a cross-sectional analysis of 1018 HIV and 1092 HIV men enrolled in the multicenter AIDS cohort study, Poisson regression with robust variance determined associations between HIV serostatus and metabolic health prevalence (defined as meeting ≤2 of 5 National Cholesterol Education Program Adult Treatment Panel III metabolic syndrome criteria), adjusting for age, race, BMI category, smoking, and hepatitis C virus infection status. RESULTS HIV men were younger (54 vs. 59 years) and had lower median BMI (25 vs. 27 kg/m). Nonobese HIV men had lower metabolic health prevalence than HIV men (BMI ≤25 kg/m: 80 vs. 94%, P < 0.001; BMI 25-29 kg/m: 64 vs. 71%, P = 0.05), but metabolic health prevalence among obese men did not differ by HIV serostatus (BMI 30-34 kg/m: 35 vs. 39%, P = 0.48; BMI ≥35 kg/m: 27 vs. 25%, P = 0.79). In the adjusted model, nonobese HIV men were less likely to demonstrate metabolic health than nonobese HIV men. Among HIV men, per year darunavir, zidovudine, and stavudine use were associated with lower metabolic health likelihood. CONCLUSION Metabolically healthy obesity prevalence does not differ by HIV serostatus. However, among nonobese men, HIV infection is associated with lower metabolic health prevalence, with associations between lack of metabolic health and darunavir and thymidine analog nucleoside reverse transcriptase inhibitor exposure observed.
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Molecular Paths Linking Metabolic Diseases, Gut Microbiota Dysbiosis and Enterobacteria Infections.
Serino, M
Journal of molecular biology. 2018;(5):581-590
Abstract
Alterations of both ecology and functions of gut microbiota are conspicuous traits of several inflammatory pathologies, notably metabolic diseases such as obesity and type 2 diabetes. Moreover, the proliferation of enterobacteria, subdominant members of the intestinal microbial ecosystem, has been shown to be favored by Western diet, the strongest inducer of both metabolic diseases and gut microbiota dysbiosis. The inner interdependence between the host and the gut microbiota is based on a plethora of molecular mechanisms by which host and intestinal microbes modify each other. Among these mechanisms are as follows: (i) the well-known metabolic impact of short chain fatty acids, produced by microbial fermentation of complex carbohydrates from plants; (ii) a mutual modulation of miRNAs expression, both on the eukaryotic (host) and prokaryotic (gut microbes) side; (iii) the production by enterobacteria of virulence factors such as the genotoxin colibactin, shown to alter the integrity of host genome and induce a senescence-like phenotype in vitro; (iv) the microbial excretion of outer-membrane vesicles, which, in addition to other functions, may act as a carrier for multiple molecules such as toxins to be delivered to target cells. In this review, I describe the major molecular mechanisms by which gut microbes exert their metabolic impact at a multi-organ level (the gut barrier being in the front line) and support the emerging triad of metabolic diseases, gut microbiota dysbiosis and enterobacteria infections.
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Branched Chain Amino Acids in Metabolic Disease.
Arany, Z, Neinast, M
Current diabetes reports. 2018;(10):76
Abstract
PURPOSE OF REVIEW Elevations in circulating branched chain amino acids (BCAAs) have gained attention as potential contributors to the development of insulin resistance and diabetes. RECENT FINDINGS Epidemiological evidence strongly supports this conclusion. Suppression of BCAA catabolism in adipose and hepatic tissues appears to be the primary drivers of plasma BCAA elevations. BCAA catabolism may be shunted to skeletal muscle, where it indirectly leads to FA accumulation and insulin resistance, via a number of proposed mechanisms. BCAAs have an important role in the development of IR, but our understanding of how plasma BCAA elevations occur, and how these elevations lead to insulin resistance, is still limited.
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Gut Microbes and Health: A Focus on the Mechanisms Linking Microbes, Obesity, and Related Disorders.
Rastelli, M, Knauf, C, Cani, PD
Obesity (Silver Spring, Md.). 2018;(5):792-800
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Abstract
The past decade has been characterized by tremendous progress in the field of the gut microbiota and its impact on host metabolism. Although numerous studies show a strong relationship between the composition of gut microbiota and specific metabolic disorders associated with obesity, the key mechanisms are still being studied. The present review focuses on specific complex pathways as well as key interactions. For instance, the nervous routes are explored by examining the enteric nervous system, the vagus nerve, and the brain, as well as the endocrine routes (i.e., glucagon-like peptide-1, peptide YY, endocannabinoids) by which gut microbes communicate with the host. Moreover, the key metabolites involved in such specific interactions (e.g., short chain fatty acids, bile acids, neurotransmitters) as well as their targets (i.e., receptors, cell types, and organs) are briefly discussed. Finally, the review highlights the role of metabolic endotoxemia in the onset of metabolic disorders and the implications for alterations in gut microbiota-host interactions and ultimately the onset of diseases.
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Prenatal vitamin D status and offspring's growth, adiposity and metabolic health: a systematic review and meta-analysis.
Santamaria, C, Bi, WG, Leduc, L, Tabatabaei, N, Jantchou, P, Luo, ZC, Audibert, F, Nuyt, AM, Wei, SQ
The British journal of nutrition. 2018;(3):310-319
Abstract
In this systematic review and meta-analysis of observational studies, we aimed to estimate the associations between prenatal vitamin D status and offspring growth, adiposity and metabolic health. We searched the literature in human studies on prenatal vitamin D status and offspring growth in PubMed, up to July 2017. Studies were selected according to their methodological quality and outcomes of interest (anthropometry, fat mass and diabetes in offspring). The inverse variance method was used to calculate the pooled mean difference (MD) with 95 % CI for continuous outcomes, and the Mantel-Haenszel method was used to calculate the pooled OR with 95 % CI for dichotomous outcomes. In all, thirty observational studies involving 35 032 mother-offspring pairs were included. Vitamin D status was evaluated by circulating 25-hydroxyvitamin D (25(OH)D) level. Low vitamin D status was based on each study's cut-off for low 25(OH)D levels. Low prenatal vitamin D levels were associated with lower birth weight (g) (MD -100·69; 95 % CI -162·25, -39·13), increased risk of small-for-gestational-age (OR 1·55; 95 % CI 1·16, 2·07) and an elevated weight (g) in infant at the age of 9 months (g) (MD 119·75; 95 % CI 32·97, 206·52). No associations were observed between prenatal vitamin D status and other growth parameters at birth, age 1 year, 4-6 years or 9 years, nor with diabetes type 1. Prenatal vitamin D may play a role in infant adiposity and accelerated postnatal growth. The effects of prenatal vitamin D on long-term metabolic health outcomes in children warrant future studies.
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Marine Omega-3 Fatty Acids, Complications of Pregnancy and Maternal Risk Factors for Offspring Cardio-Metabolic Disease.
Phang, M, Skilton, MR
Marine drugs. 2018;(5)
Abstract
Marine omega-3 polyunsaturated fatty acids (n-3 PUFA) are important nutrients during periods of rapid growth and development in utero and infancy. Maternal health and risk factors play a crucial role in birth outcomes and subsequently offspring cardio-metabolic health. Evidence from observational studies and randomized trials have suggested a potential association of maternal intake of marine n-3 PUFAs during pregnancy with pregnancy and birth outcomes. However, there is inconsistency in the literature on whether marine n-3 PUFA supplementation during pregnancy can prevent maternal complications of pregnancy. This narrative literature review summarizes recent evidence on observational and clinical trials of marine n-3 PUFA intake on maternal risk factors and effects on offspring cardio-metabolic health. The current evidence generally does not support a role of maternal n-3 PUFA supplementation in altering the incidence of gestational diabetes, pregnancy-induced hypertension, or pre-eclampsia. It may be that benefits from marine n-3 PUFA supplementation are more pronounced in high-risk populations, such as women with a history of complications of pregnancy, or women with low marine n-3 PUFA intake. Discrepancies between studies may be related to differences in study design, dosage, fatty acid interplay, and length of treatment. Further prospective double-blind studies are needed to clarify the impact of long-chain marine n-3 PUFAs on risk factors for cardio-metabolic disease in the offspring.
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Outcomes of mitochondrial derived diseases: a single-center experience.
Erdol, S, Saglam, H
Journal of pediatric endocrinology & metabolism : JPEM. 2018;(4):399-405
Abstract
BACKGROUND The purpose of this study is to help elucidate which part of the mitochondria is causing a problem through anamnesis, physical examination, and routine biochemical tests in the event of a suspected mitochondrial disease case. METHODS The data were obtained retrospectively from the medical records of 75 cases; the mitochondrial-derived disease (MDD) cases were observed in our center from 2011 to 2017. RESULTS The most commonly observed MDDs were oxidative phosphorylation disorders at 44%, followed by fatty acid oxidation disorder at 40%, pyruvate metabolism disorder at 12%, and ketone metabolism disorder at 4%, respectively. The most common clinical presentation at the time of referral to the hospital was metabolic acidosis (20%), and the most common symptom was respiratory distress (24%). There were abnormal findings in 84.3% of the cases subjected to cranial magnetic resonance imaging (MRI), with the most common being hyperintensity in the bilateral basal ganglia (49.0%). CONCLUSIONS Anamnesis, physical examination, and simple laboratory data could provide some important clues in assessing MDD. Blood gas should definitely be measured in cases with respiratory symptoms, particularly if they have a history of consanguineous marriage or a sibling suffering from a similar disease. If metabolic acidosis exists in the blood gas, MDDs should absolutely be included in the differential diagnosis. Furthermore, ophthalmic and cardiac assessment and cranial MRI will also reveal significant data for diagnosing MDDs.
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Are heterozygous carriers for hereditary fructose intolerance predisposed to metabolic disturbances when exposed to fructose?
Debray, FG, Damjanovic, K, Rosset, R, Mittaz-Crettol, L, Roux, C, Braissant, O, Barbey, F, Bonafé, L, De Bandt, JP, Tappy, L, et al
The American journal of clinical nutrition. 2018;(2):292-299
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Abstract
BACKGROUND High fructose intake causes hepatic insulin resistance and increases postprandial blood glucose, lactate, triglyceride, and uric acid concentrations. Uric acid may contribute to insulin resistance and dyslipidemia in the general population. In patients with hereditary fructose intolerance, fructose consumption is associated with acute hypoglycemia, renal tubular acidosis, and hyperuricemia. OBJECTIVE We investigated whether asymptomatic carriers for hereditary fructose intolerance (HFI) would have a higher sensitivity to adverse effects of fructose than would the general population. DESIGN Eight subjects heterozygous for HFI (hHFI; 4 men, 4 women) and 8 control subjects received a low-fructose diet for 7 d and on the eighth day ingested a test meal, calculated to provide 25% of the basal energy requirement, containing 13C-labeled fructose (0.35 g/kg), glucose (0.35 g/kg), protein (0.21 g/kg), and lipid (0.22 g/kg). Glucose rate of appearance (GRa, calculated with [6,6-2H2]glucose), fructose, net carbohydrate, and lipid oxidation, and plasma triglyceride, uric acid, and lactate concentrations were monitored over 6 h postprandially. RESULTS Postprandial GRa, fructose, net carbohydrate, and lipid oxidation, and plasma lactate and triglyceride concentrations were not significantly different between the 2 groups. Postprandial plasma uric acid increased by 7.2% compared with fasting values in hHFI subjects (P < 0.01), but not in control subjects (-1.1%, ns). CONCLUSIONS Heterozygous carriers of hereditary fructose intolerance had no significant alteration of postprandial fructose metabolism compared with control subjects. They did, however, show a postprandial increase in plasma uric acid concentration that was not observed in control subjects in responses to ingestion of a modest amount of fructose. This trial was registered at the US Clinical Trials Registry as NCT02979106.
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Effects of alternate day calorie restriction and exercise on cardio-metabolic risk factors in overweight and obese adults: an exploratory randomized controlled study.
Oh, M, Kim, S, An, KY, Min, J, Yang, HI, Lee, J, Lee, MK, Kim, DI, Lee, HS, Lee, JW, et al
BMC public health. 2018;(1):1124
Abstract
BACKGROUND It has been recognized that alternate day calorie restriction (ADCR) or exercise has positive effects on cardio-metabolic risk factors. It is unclear whether the combined effect of ADCR and exercise (aerobic + resistance training) influences risk. We investigated effects of an 8-week ADCR and exercise program (aerobic + resistance training) on cardio-metabolic risk factors in overweight and obese adults. METHODS This study randomized 45 overweight or obese but healthy adults (F = 26, M = 19; aged about 32 to 40 years) into 4 groups: ADCR (n = 13), exercise (n = 10), exercise plus ADCR (n = 12), and control (n = 10) for 8 weeks. Body composition, blood lipids profile, and insulin resistance were measured. The intention to treat (ITT) method was used to analyze all participants that were randomized. RESULTS A total of 35 participants completed the trial (78%). Body weight, body mass index, waist circumference, fat mass and percent body fat were reduced in the exercise plus ADCR group (- 3.3 ± 2.4 kg, p < 0.01; - 1.3 ± 1.0 kg/m2, p < 0.01; - 4.1 ± 3.9 cm, p < 0.01; - 2.7 ± 2.0 kg, p < 0.01; - 2. 5 ± 2.2%, p < 0.01). Insulin, glucose, homeostasis model assessment insulin resistance and triglyceride (- 2.9 ± 4.1 μIU/ml, p < 0.05; - 10.9 ± 16.9 mg/dl, p < 0.05; - 0.9 ± 1.3, p < 0.05; - 43.8 ± 41.9 mg/dl, p < 0.01) decreased in the exercise plus ADCR group only. CONCLUSIONS ADCR and exercise both proved to be beneficial, but the combined intervention was most effective at inducing beneficial changes in body weight, body composition, glucose, insulin, insulin resistance and triglyceride in overweight and obese adults. TRIAL REGISTRATION ClinicalTrials.gov: NCT03652532 , Registered August 28, 2018, 'retrospectively registered'.
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The relation of vitamin D, metabolic risk and negative symptom severity in people with psychotic disorders.
Bruins, J, Jörg, F, van den Heuvel, ER, Bartels-Velthuis, AA, Corpeleijn, E, Muskiet, FAJ, Pijnenborg, GHM, Bruggeman, R
Schizophrenia research. 2018;:513-518