Markers Of Glucose Metabolism Research Articles

Pretreatment Prevotella-to-Bacteroides ratio and markers of glucose metabolism as prognostic markers for dietary weight loss maintenance.

Pre-treatment gut microbial Prevotella-to-Bacteroides (P/B) ratio and markers of glucose metabolism (i.e., fasting glucose and insulin) have been suggested as biomarkers for optimal weight management. However, both biomarkers need further validation, and the interactions between them for optimal weight management are largely unknown. To investigate differences in weight loss maintenance between subjects with low and high P/B ratio and the potential interactions with markers of glucose metabolism and dietary fiber intake. Following an 8-week weight loss period using meal replacement products, subjects losing ≥ 8% of their initial body weight were randomized to one of three protein supplements or maltodextrin for a 24-week weight maintenance period. Habitual diet was consumed along with the supplements expected to constitute 10-15% of total energy. For this analysis we stratified the participants into low and high strata based on median values of pre-intervention P/B ratio, pre-weight loss Homeostatic model assessment of insulin resistance (HOMA-IR) (<2.33 or > 2.33), and dietary fiber intake during the intervention (< 28.5 or > 28.5 g/10 MJ). Regardless of weight maintenance regimen, subjects with high P/B ratio (n = 63) regained 1.5 (95% CI 0.4, 2.7) kg body weight (P = 0.007) more than subjects with low P/B ratio (n = 63). The regain among subjects with high P/B ratio was particular evident if HOMA-IR was high and dietary fiber intake was low. Consequently, in the high P/B strata, subjects with high HOMA-IR and low fiber intake (n = 17) regained 5.3 (95% CI 3.3, 7.3) kg (P < 0.001) more body weight compared with participants with low HOMA-IR and high fiber intake (n = 16). Subjects with high P/B ratio were more susceptible to regain body weight compared with subjects with low P/B ratio, especially when dietary fiber intake was low and glucose metabolism was impaired. These observations underline that both the P/B ratio and markers of glucose metabolism should be considered as important biomarkers within personalized nutrition for optimal weight management.

Protective effects of melatonin on sepsis-induced liver injury and dysregulation of gluconeogenesis in rats through activating SIRT1/STAT3 pathway

Sepsis, a life-threatening disease with high morbidity and mortality in critically ill patients, usually leads to serious complications including liver damage and dysregulated metabolic homoeostasis. The aim of this study was to evaluate the therapeutic potential of melatonin in rats with caecal ligation and puncture (CLP)-induced sepsis, which mimics critical infections in humans and explore the underlying molecular mechanisms. Male Sprague-Dawley rats received CLP surgery under anaesthesia to induce polymicrobial sepsis. Melatonin (20 mg/kg) was intraperitoneally (i.p.) injected every 12 h for 7 days after CLP, with or without intraperitoneal injection of the SIRT1 inhibitor EX527 (5 mg/kg). Markers of glucose metabolism, inflammation, liver function and associated signaling pathway were measured. Septic rats exhibited marked inhibition of the hepatic SIRT1/STAT3 pathway, along with increased blood glucose levels and hepatic gluconeogenesis. Melatonin administration efficiently attenuated liver dysfunction and glucose metabolism disorders by promoting hepatic SIRT1 expression and STAT3 phosphorylation. Furthermore, inhibition of SIRT1 by EX527 significantly diminished the protective effects of melatonin on sepsis induced liver injury, hyperglycaemia and STAT3 inactivation. These results emphasize that melatonin is a potential therapeutic agent for sepsis-associated liver injury and glucose metabolism disorders, possibly acting by targeting SIRT1-mediated STAT3 activation in the liver.

The relationship between serum FGF-23 concentration and insulin resistance, prediabetes and dyslipidemia in obese children and adolescents.

Background Obesity is known to cause metabolic disturbances including insulin resistance, dyslipidemia and alters bone mineralization. The effects of obesity on fibroblast growth factor 23 (FGF-23), which is important in bone mineralization, have not yet been clarified. Our aim was to investigate the association between FGF-23 concentration and obesity-associated dysmetabolism. Methods Subjects comprised 46 obese children and adolescents. The same number of age-matched, healthy controls were recruited. Markers of bone mineralization and glucose metabolism were measured. Thyroid function and insulin resistance were investigated in both groups. In obese subjects; an oral glucose tolerance test (OGTT) was performed and hemoglobin A1c and lipid fractions were measured. Bone mineral density and hepatic steatosis were investigated. Results Serum FGF-23, α-klotho and 1,25(OH)2D3 concentrations were significantly lower while fasting insulin, fasting glucose, C-peptide and alkaline phosphatase (ALP) concentrations and homeostasis model assessment of insulin resistance (HOMA-IR) were significantly higher in the obese group compared to controls. A significant negative correlation was observed between free tri-iodothyronine (fT3) and both FGF-23 and α-klotho in the obese group. Significant negative correlation was found between FGF-23 and C-peptide and a positive correlation was found between FGF-23 and high density lipoprotein-cholesterol (HDL-c) in the obese subjects with impaired glucose tolerance (IGT). Significant negative correlations were found between FGF-23 and both fasting insulin levels and C-peptide levels in the obese subjects with hepatic steatosis. Conclusions In our study, insulin resistance-associated hyperinsulinism and/or lower 1,25(OH)2D3 levels, both present in obese children and adolescents, may lead to decreased serum FGF-23 concentrations in obese subjects.

Effects of nut and seed consumption on markers of glucose metabolism in adults with prediabetes: a systematic review of randomised controlled trials.

The primary aim was to investigate the effects of nut and seed consumption on markers of glucose metabolism in adults with prediabetes. Studies with a randomised controlled trial (RCT) design, comparing the effects of a diet containing nuts or seeds against a diet without nuts or seeds in adults with prediabetes, were considered eligible. Primary outcome measures included fasting plasma glucose (FPG), 2-h plasma glucose during oral glucose tolerance test and glycated Hb (HbA1c) concentrations. Studies were identified by searching PubMed and Scopus electronic databases and by checking full texts and reference lists of relevant records. Risk of bias was assessed using the Cochrane Collaboration's tool. We included five RCT involving 371 adults with prediabetes or at risk of diabetes; three RCT investigated the effects of whole nut consumption and two the effects of ground flaxseed consumption. Consumption of 57g/d pistachios or mean intake of 60g/d almonds for 4months improved FPG and fasting plasma insulin (FPI) concentrations, insulin resistance, cellular glucose uptake in lymphocytes and β-cell function. Consumption of 56g/d walnuts for 6months was not found to affect FPG or HbA1c concentrations. Consumption of 13g/d flaxseed for 3months improved FPG and FPI concentrations and insulin resistance. In a second study, however, flaxseed consumption was not found to affect markers of glucose metabolism. The risk of bias was generally low, thus the reported results could be reliable. Further investigation of nut and seed consumption effects in the field of prediabetes is warranted.

Thyroid function, body mass index, and metabolic risk markers in euthyroid adults: a cohort study

BackgroundIn recent years, the relationship between thyroid stimulating hormone (TSH) and obesity has been widely discussed. However, it is unclear how thyroid hormone concentrations relate to body weight and its impact on metabolic risk markers. This study aimed to assess how thyroid function is linked to underweight, overweight, or obesity, and metabolic risk markers in adults.MethodsA total of 16,975 subjects, aged 18–80 years, who attended the Health Management Center of Tongji Hospital, Wuhan, China were enrolled in this study. Anthropometric and laboratory data were collected and analyzed.ResultsSerum free triiodothyronine (fT3) and fT3/free thyroxine (fT4) ratio (fT3/fT4) were positively associated with body mass index (BMI) (P < 0.001), while there was a negative relationship between fT4 and BMI (P < 0.001) according to multivariable regression analysis adjusted for age and sex. Associations between thyroid hormone concentrations and markers of blood pressure, and lipid and glucose metabolism were identified after adjustment for age, sex, and BMI, with TSH being negatively associated with fasting blood glucose (FBG). fT3 was positively associated with systolic blood pressure and low-density lipoprotein-cholesterol, while fT4 was positively associated with diastolic blood pressure, FBG, and high-density lipoprotein-cholesterol (HDL-C), and negatively associated with hemoglobin A1c (HbA1c) and triglyceride. Finally, fT3/fT4 was positively associated with HbA1c and triglyceride, and negatively associated with HDL-C.ConclusionsOverweight or obese participants had a high serum concentration of fT3, high fT3/fT4 ratio, and a low concentration of fT4. Underweight participants had high concentrations of fT4 and low concentrations of fT3. Thus, relationships between thyroid hormones and metabolic risk markers were identified which suggest that thyroid function might be one factor that influences body weight and the co-morbidities of obesity.

2060-P: Serum Wnt Inhibitor DKK1 Is Associated with Adiposity and Insulin Resistance in Nondiabetic North Americans

Background: The Wnt pathway is known to influence body composition during early human development by regulating bone formation, myogenesis and adipogenesis. We have recently shown that DKK1 is related to measures of adiposity in nondiabetic African ancestry males. Whether these relationships are true across sexes and/or in other human populations remains unknown. In this study we evaluated the relationship of DKK1 with adiposity in a sample of male and female, mixed race, nondiabetic North American individuals. Methods: Fasting serum DKK1 levels were measured using ELISAs in 201 nondiabetic subjects (age range 30.7-60 years, BMI range 19.9-64.0 kg/m2) recruited from the general population via television advertisement and mass mailing. The subjects were predominantly female (85%) and Caucasian (63%). Anthropometrics were obtained and markers of inflammation and glucose metabolism were measured from fasting serum samples. Spearman and partial Spearman correlation analysis was used to determine the association of DKK1 with measures of adiposity and insulin resistance. Results: Circulating DKK1 was positively associated with BMI (r=0.30, p&amp;lt;0.001) and waist circumference (r=0.25, p&amp;lt;0.001), independent of age, race and sex. In addition, DKK1 was positively associated with fasting serum insulin level (r=0.18, p&amp;lt;0.01) and HOMA-IR (r=0.19, p&amp;lt;0.01) in age, sex and race adjusted models. However, these associations were no longer significant after adjustment for BMI. Conclusion: This is the first study looking at correlation of DKK1 with adiposity in North American nondiabetic individuals. Our findings suggest that the link between DKK1 and insulin resistance maybe mediated indirectly through total and regional adiposity and that DKK1 could be a potential early biomarker for diabetes in high risk individuals. These findings support our findings in African ancestry males and add to the evidence favoring potential role of Wnt modulators in adiposity regulation in humans. Disclosure H. Ali: None. E. Oczypok: None. I. Miljkovic: None. R. Cvejkus: None. J.M. Zmuda: None. J. DeLany: None. E.E. Kershaw: Research Support; Self; Regeneron Pharmaceuticals. Funding National Institutes of Health (T32DK007252); Endocrine Fellows Foundation

Urinary bisphenol A concentration and glucose homeostasis in non-diabetic adults: a repeated-measures, longitudinal study.

Bisphenol A (BPA) has been shown to be potentially associated with type 2 diabetes; however, there is little evidence associating BPA exposure with glucose metabolic outcomes prior to diabetes onset. We aimed to examine BPA exposure in relation to glucose homeostasis among non-diabetic individuals. This longitudinal cohort study comprised 2336 Chinese adults aged 40years or above (62.8% women) and free of diabetes at baseline in 2009, followed for 4years. Urinary BPA and glucose metabolic traits including fasting plasma glucose (FPG), 2h post-load plasma glucose, fasting serum insulin, HOMA-IR and HOMA-B were measured at baseline and follow-up. Repeated-measures analysis was performed to evaluate associations of urinary BPA concentration with markers of glucose homeostasis. After full adjustment for confounders including BMI, each tenfold increase in urinary BPA concentrations was associated with a 3.39% increase in FPG (95% CI 2.24%, 4.55%) and an 11.6% decrease in HOMA-B (95% CI -15.8%, -7.18%) in women. The inverse association between urinary BPA and HOMA-B was more prominent among overweight or obese individuals (change -13.7%; 95% CI -19.3%, -7.61%) compared with those who were of normal weight (change -6.74%; 95% CI -13.2%, 0.20%) (pinteraction = 0.07). Moreover, the ORs of fasting hyperglycaemia and beta cell dysfunction corresponding to a tenfold increase in urinary BPA concentrations were 1.37 (95% CI 1.10, 1.72) and 1.30 (95% CI 1.02, 1.65) in women, respectively. No significant associations existed between urinary BPA and glucose metabolic markers in men. Our findings suggest that exposure to BPA was independently associated with impaired glucose homeostasis before the development of diabetes in middle-aged and elderly women.

Lysosomal Acid Lipase as a Molecular Target of the Very Low Carbohydrate Ketogenic Diet in Morbidly Obese Patients: The Potential Effects on Liver Steatosis and Cardiovascular Risk Factors.

A very low carbohydrate ketogenic diet (VLCKD) is an emerging technique to induce a significant, well-tolerated, and rapid loss of body weight in morbidly obese patients. The low activity of lysosomal acid lipase (LAL) could be involved in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), which is a common feature in morbidly obese patients. Fifty-two obese patients suitable for a bariatric surgery intervention underwent a 25-day-long VLCKD. The biochemical markers of glucose and lipid metabolism, and flow-mediated dilation (FMD) of the brachial artery were measured before and after VLCKD. LAL activity was measured using the dried blood spot technique in 20 obese patients and in a control group of 20 healthy, normal-weight subjects. After VLCKD, we observed a significant reduction in body mass index, fasting glucose, insulinemia, and lipid profile parameters. No significant variation in FMD was observed. The number of patients with severe liver steatosis significantly decreased. LAL activity significantly increased, although the levels were not significantly different as compared to the control group. In conclusion, VLCKD induces the activity of LAL in morbidly obese subjects and reduces the secretion of all circulating lipoproteins. These effects could be attributed to the peculiar composition of the diet, which is particularly poor in carbohydrates and relatively rich in proteins.

Gut bacteria are critical for optimal muscle function: a potential link with glucose homeostasis.

Gut microbiota is involved in the development of several chronic diseases, including diabetes, obesity, and cancer, through its interactions with the host organs. It has been suggested that the cross talk between gut microbiota and skeletal muscle plays a role in different pathological conditions, such as intestinal chronic inflammation and cachexia. However, it remains unclear whether gut microbiota directly influences skeletal muscle function. In this work, we studied the impact of gut microbiota modulation on mice skeletal muscle function and investigated the underlying mechanisms. We determined the consequences of gut microbiota depletion after treatment with a mixture of a broad spectrum of antibiotics for 21 days and after 10 days of natural reseeding. We found that, in gut microbiota-depleted mice, running endurance was decreased, as well as the extensor digitorum longus muscle fatigue index in an ex vivo contractile test. Importantly, the muscle endurance capacity was efficiently normalized by natural reseeding. These endurance changes were not related to variation in muscle mass, fiber typology, or mitochondrial function. However, several pertinent glucose metabolism markers, such as ileum gene expression of short fatty acid chain and glucose transporters G protein-coupled receptor 41 and sodium-glucose cotransporter 1 and muscle glycogen level, paralleled the muscle endurance changes observed after treatment with antibiotics for 21 days and reseeding. Because glycogen is a key energetic substrate for prolonged exercise, modulating its muscle availability via gut microbiota represents one potent mechanism that can contribute to the gut microbiota-skeletal muscle axis. Taken together, our results strongly support the hypothesis that gut bacteria are required for host optimal skeletal muscle function.

Activity and molecular targets of pioglitazone via blockade of proliferation, invasiveness and bioenergetics in human NSCLC

BackgroundPioglitazone, a synthetic peroxisome proliferator activated receptor (PPAR-γ) ligand, is known as an antidiabetic drug included in the thiazolidinediones (TZDs) class. It regulates the lipid and glucose cell metabolism and recently a role in the inhibition of numerous cancer cell processes has been described.MethodsIn our work we investigate the anti-tumor effects of pioglitazone in in vitro models of non small cell lung cancer (NSCLC) and also, we generated ex-vivo three-dimensional (3D) cultures from human lung adenocarcinoma (ADK) as a model to test drug efficacy observed in vitro. The inhibitory effect of pioglitazone on cell proliferation, apoptosis and cell invasion in a panel of human NSCLC cell lines was evaluated by multiple assays.ResultsPioglitazone reduced proliferative and invasive abilities with an IC50 ranging between 5 and 10 μM and induced apoptosis of NSCLC cells. mRNA microarray expression profiling showed a down regulation of MAPK, Myc and Ras genes after treatment with pioglitazone; altered gene expression was confirmed by protein analysis in a dose-related reduction of survivin and phosphorylated proteins levels of MAPK pathway. Interestingly mRNA microarray analysis showed also that pioglitazone affects TGFβ pathway, which is important in the epithelial-to-mesenchimal transition (EMT) process, by down-regulating TGFβR1 and SMAD3 mRNA expression. In addition, extracellular acidification rate (ECAR) and a proportional reduction of markers of altered glucose metabolism in treated cells demonstrated also cell bioenergetics modulation by pioglitazone.ConclusionsData indicate that PPAR-γ agonists represent an attractive treatment tool and by suppression of cell growth (in vitro and ex vivo models) and of invasion via blockade of MAPK cascade and TGFβ/SMADs signaling, respectively, and its role in cancer bioenergetics and metabolism indicate that PPAR-γ agonists represent an attractive treatment tool for NSCLC.

Change of Glucose Metabolism and Fibrosis Markers in Patients With Hepatitis C Under Treatment With Antiviral Agents

Change of Glucose Metabolism and Fibrosis Markers in Patients With Hepatitis C Under Treatment With Antiviral Agents

Markers of bone turnover are reduced in patients with CF related diabetes; the role of glucose

BackgroundCystic fibrosis(CF) related diabetes(CFRD) and osteoporosis are prevalent in adult patients with CF. We aimed to evaluate if CFRD and markers of glucose metabolism and inflammation are associated with bone turnover in CF. MethodsCross sectional study at the adult section at the Copenhagen CF Center from January–October 2017. Fasting blood samples, including bone turnover markers(BTMs) and cytokines, Dual-x-ray absorptiometry scan and oral glucose tolerance test were performed. Lung-transplanted participants and patients in antiosteoporotic treatment were excluded from analyses. Results102 patients were included of whom 19 had a prior CFRD diagnosis. CFRD patients had lower procollagen type 1 N-terminal propeptide(P1NP) and C-Terminal cross-linked Telopeptide(CTX) levels compared to CF patients without diabetes (median[IQR]) 49.5 μg/l [29.6,57.1] vs 56.9 μg/l [38.2,74.3], p = .03 and 0.2 μg/l [0.1,0.3] vs 0.4 μg/l [0.3,0.6], p < .01, respectively. Fasting plasma glucose(FPG) was negatively associated with the bone formation markers P1NP and osteocalcin and bone resorption marker CTX. In multivariate linear regression FPG remained a significant predictor of P1NP -1.07 [−1.09;-0.01] and CTX -1.13 [−1.21;-1.06]. Bone mineral density Z-score was not different between patients with and without CFRD but FPG was negatively associated with hip and femoral neck Z-score. There was no consistent association between inflammatory cytokines and BTMs. ConclusionsBone turnover markers are reduced in CF patients with CFRD and negatively associated with glucose levels. Extra attention towards frequent hyperglycemia in CF patients should be taken when evaluating decreased BMD. Glycemia may be a future target for improving outcome in CFBD.

Effects of Cold-inducible RNA-binding Protein (CIRP) on Liver Glycolysis during Acute Cold Exposure in C57BL/6 Mice.

Cold-inducible RNA-binding protein (CIRP) is a stress-responsive protein involved in several signal transduction pathways required for cellular function, which are associated with apoptosis and proliferation. The present study aimed to investigate the possible effects of CIRP-mediated regulation of glucose metabolism in the liver following acute cold exposure. The livers and serum of male C57BL/6 mice were collected following cold exposure at 4 °C for 0 h, 2 h, 4 h, and 6 h. Glucose metabolic markers and the expression of glucose metabolic-related proteins were detected in the liver. Acute cold exposure was found to increase the consumption of glycogen in the liver. Fructose-1,6-diphosphate (FDP) and pyruvic acid (PA) were found to show a brief increase followed by a sharp decrease during cold exposure. Anti-apoptotic protein (Bcl-2) expression was upregulated. CIRP protein expression displayed a sequential increase with prolonged acute cold exposure time. Acute cold exposure also increased the level of protein kinase B (AKT) phosphorylation, and activated the AKT-signaling pathway. Taken together, these findings indicate that acute cold exposure increased the expression of CIRP protein, which regulates mouse hepatic glucose metabolism and maintains hepatocyte energy balance through the AKT signaling pathway, thereby slowing the liver cell apoptosis caused by cold exposure.

Role of Theobromine in Cocoa's Metabolic Properties in Healthy Rats.

Cocoa is rich in polyphenols and methylxanthines, and it has been reported that its consumption, among other properties, has beneficial effects on metabolism. This study aimed to investigate the role of theobromine in cocoa's metabolic properties in healthy rats. In addition to morphometric measurements, biochemical markers of lipids and glucose metabolism and gene expression of molecules related to immune cells in adipose and hepatic tissues were assessed after 7 or 18 days of diet. Additionally, a metabolomic analysis was carried out at day 7. This study revealed the presence of six discriminant metabolites in plasma due to the diets. Moreover, the results showed that theobromine is the main responsiblefactor for cocoa's effects on body weight gain as well as on lipid and glucose metabolism. The effects on body weight and lipids appeared as early as after 7 days of diet, whereas those affecting glucose metabolism required a longer intervention.

Serum Calcium Concentrations, Chronic Inflammation and Glucose Metabolism: A Cross-Sectional Analysis in the Andhra Pradesh Children and Parents Study (APCaPS)

BackgroundEvidence suggests a role for elevated serum calcium in dysregulated glucose metabolism, linked through low-level chronic inflammation. ObjectivesWe investigated the association of elevated serum calcium concentrations (corrected for albumin) with markers of dysregulated glucose metabolism and type II diabetes and tested if these associations were accounted for by chronic inflammation in a rural Indian population. MethodsA cross-sectional analysis of participants aged 40–84 y from the Andhra Pradesh Children and Parents Study (APCaPS; n = 2699, 52.2% women) was conducted. Comprehensive information on household, sociodemographic, and lifestyle factors; medical and family history; physical measurements; blood measurements including fasting plasma glucose (FPG), fasting insulin (FI), serum calcium, albumin, phosphorous, vitamin D (in a subset), and creatinine were analyzed. Additionally, in a random sample of healthy participants (n = 1000), inflammatory biomarkers (interleukins 6 and 18, soluble intercellular adhesion molecule 1, adiponectin, and high-sensitivity C-reactive protein) were measured and an inflammatory score (IScore) calculated. ResultsAfter adjustments for sociodemographics, lifestyle factors, and anthropometry the highest calcium quartile (Q4 compared with Q1) was associated with FI (β = 1.4 µU/ml; 95% CI: 1.2, 1.5 µU/ml; P-trend < 0.001), the homeostasis model assessment for insulin resistance (HOMA-IR) (β = 1.4; 95% CI: 1.2, 1.5; P-trend < 0.001), and was modestly associated with FPG (β = 2.1 mg/dL; 95% CI: −0.9, 5.2 mg/dL; P-trend = 0.058) and prevalent type II diabetes (OR = 1.6; 95% CI: 1.0, 2.6; P-trend= 0.020). In the healthy subgroup, the association of the highest calcium quartile was similar for FI and HOMA-IR. Additional adjustment with IScore did not alter the associations. Further, in a subset, all these associations were independent of endogenous regulators of calcium metabolism (serum vitamin D, phosphorus, and creatinine). Independently, after accounting for potential confounders, the highest IScore quartile (Q4 compared with Q1) was positively associated with FPG, FI, HOMA-IR, and prevalent prediabetes, and also with serum calcium concentrations in men. ConclusionsElevated serum calcium was positively associated with markers of dysregulated glucose metabolism and prevalent type II diabetes in a rural Indian population. Chronic inflammation did not mediate this association but was independently associated with markers of dysregulated glucose metabolism. Inflammation might be responsible for elevated serum calcium concentrations in men.

Fish protein supplementation in older nursing home residents: a randomised, double-blind, pilot study

BackgroundAge-related loss of muscle mass and function is common in older adults, and studies investigating if dietary proteins may protect and possibly build lean body mass are needed. We assessed the feasibility of conducting a nutritional intervention study in older nursing home residents to investigate the effects of fish protein supplementation on markers of glucose metabolism and inflammation.MethodsThis was a double-blind randomised controlled pilot study. Twenty-four nursing home residents, without major cognitive impairment, received a daily oral nutritional supplement containing 5.2 g of fish protein or placebo for 6 weeks. Anthropometric measurements were conducted at baseline. Participants were screened for nutritional risk using the Mini Nutritional Assessment and activities of daily living using the Barthel index and dietary intake was registered. Hand grip strength was measured and fasting blood samples collected at baseline and endpoint.ResultsCompliance was high and dropout was low, but participant recruitment was challenging. Serum concentrations of monocyte chemoattractant protein-1 decreased, and C-reactive protein increased in the intervention group compared to control, with no changes in markers of glucose metabolism between groups.ConclusionConducting a nutritional intervention using fish protein supplementation in older nursing home residents is feasible but should be conducted as a multi-centre study to account for the low recruitment rate observed in the present study. A full-scale study is needed to gain more knowledge on the potential effects of fish proteins on markers of glucose metabolism and inflammation in relation to the age-related loss of muscle mass and function.Trial registrationClinicalTrials.gov NCT03529344 18.05.2018 (retrospectively registered)

A Single Dose of Goji Berries Does Not Affect Postprandial Energy Expenditure and Substrate Oxidation in Healthy, Overweight Men.

Background and Aim Increasing energy expenditure is an effective strategy for the prevention of obesity. In this respect, Lycium barbarum (goji berry) is of interest, as it has been shown to increase postprandial oxygen consumption. Although this suggests that energy expenditure was also increased, energy expenditure and substrate oxidation can only be assessed accurately when both oxygen consumption and carbon dioxide production are measured. We therefore investigated the effects of a single dose of Lycium barbarum fruit on postprandial energy expenditure and substrate oxidation in a randomized, double-blind crossover trial. In addition, markers of lipid and glucose metabolism were measured. Methods Seventeen healthy, overweight men received in a random order a meal containing 25 grams of dried Lycium barbarum fruit or a control meal matched for caloric content and macronutrient composition. Energy expenditure and the respiratory quotient were determined using indirect calorimetry before and up to 4 hours after meal intake. Blood was sampled before and after meal intake at regular intervals for analyses of plasma glucose, serum triacylglycerol, and free fatty acid concentrations. Results Energy expenditure significantly increased after the Lycium barbarum and control meal, but no differences were found between the meals (p=0.217). Postprandial changes in respiratory quotient (p=0.719) and concentrations of glucose (p=0.663), triacylglycerol (p=0.391), and free fatty acids (p=0.287) were also not affected by Lycium barbarum intake. Conclusions A single dose of Lycium barbarum does not affect postprandial energy expenditure, substrate oxidation, and markers for lipid and glucose metabolism in healthy, overweight men.

Plant-derived polyunsaturated fatty acids and markers of glucose metabolism and insulin resistance: a meta-analysis of randomized controlled feeding trials

The objective of this meta-analysis was to investigate the effects of plant-derived polyunsaturated fatty acids (PUFAs) on glucose metabolism and insulin resistance. Scopus and PubMed databases were searched until January...

GDF15 reflects beta cell function in obese patients independently of the grade of impairment of glucose metabolism

Background and aimsGrowth differentiation factor 15 (GDF15) is a strong predictor of cardiovascular morbidity and mortality found to be both marker and target of impaired glucose metabolism. GDF15 increases following glucose administration and is up-regulated in obesity and diabetes. We investigate here the relationship between GDF15 and beta cell function. Methods and resultsIn this cross-sectional study we evaluated GDF15 concentrations in 160 obese subjects (BMI 35–63 kg/m2, age 39.4 ± 18.6 years, m/f 38/122) who underwent a 75 g oral glucose tolerance test (OGTT). Based on the OGTT results, the cohort was divided into two groups: 1) normal fasting glucose and normal glucose tolerance (n = 80), 2) impaired fasting glucose, impaired glucose tolerance or type 2 diabetes (n = 80). The relationship of GDF15 to fasting and OGTT-based dynamic insulin sensitivity and insulin secretion parameters was evaluated.GDF15 was higher in the prediabetes and diabetes groups and correlated with HbA1c, glucose, insulin as well as baseline and dynamic indices of insulin sensitivity and estimated beta cell function. Multiple regression analysis revealed that age, waist-to-height ratio, glomerular filtration rate and prehepatic beta cell function, but not the grade of impairment of glucose metabolism, were independent predictors of GDF15. Subgroup analysis showed that of all parameters of glucose metabolism only C-peptide, fasting prehepatic beta cell function and insulinogenic index remained significantly related to GDF15 in both groups. ConclusionWe conclude that in patients with severe obesity, GDF15 strongly relates to beta cell function and should be further investigated as a potential therapeutic target and biomarker guiding treatment options.

Effects of nanoparticles of hydroxy-aluminum phthalocyanine on markers of liver injury and glucose metabolism in diabetic mice.

Photodynamic therapy, by reducing pain and inflammation and promoting the proliferation of healthy cells, can be used to treat recurrent lesions, such as diabetic foot ulcers. Studies using the photosensitizer phthalocyanine, together with the nanostructured copolymeric matrix of Pluronic® and Carbopol® for the treatment of diabetic foot ulcers and leishmaniosis lesions, are showing promising outcomes. Despite their topical or subcutaneous administration, these molecules are absorbed and their systemic effects are unknown. Therefore, we investigated the effect of the subcutaneous administration of the hydroxy-aluminum phthalocyanine hydrogel without illumination on systemic parameters, markers of liver injury, and liver energy metabolism in type 1 diabetic Swiss mice. Both the hydrogel and the different doses of phthalocyanine changed the levels of injury markers and the liver glucose release, sometimes aggravating the alterations caused by the diabetic condition itself. However, the dose of 2.23 µg/mL caused less marked plasmatic and metabolic changes and did not change glucose tolerance or insulin sensitivity of the diabetic mice. These results are indicative that the use of hydroxy-aluminum phthalocyanine hydrogel for the treatment of cutaneous ulcers in diabetic patients is systemically safe.