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OBJECTIVES: Aronia melanocarpa (Aronia) is a shrub with small berries, chokeberries. Chokeberries are claimed to possess health benefits due to a high content of polyphenols. Aronia is known to be extremely antioxidant; however, evidence for its health benefits is not established. This review gives an overview of the impact of Aronia on cardiometabolic risk factors and diseases. METHODS: Seventeen studies on cardiometabolic risk factors and diseases were identified through a systematic search on PubMed, Embase, and Cochrane. Inclusion criteria were studies with Aronia as intervention, performed in individuals with cardiometabolic disease or risk factors, e. g., type 2 diabetes (T2D), cardiovascular disease, hypertension, dyslipidaemia, impaired glucose tolerance, overweight, central obesity and smoking. Four of these studies were applicable for a quantitative analysis. RESULTS: Aronia did not influence body weight, circulating triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, or blood pressure. The quantitative analysis revealed a mean reduction in blood glucose of 0.44 mmol/l (P=0.0001) in the treatment group compared with the control group suggesting that Aronia treatment may have a beneficial impact on blood glucose. In addition, treatment durations of 6 weeks to 3 months tended to decrease low-density lipoprotein (LDL) cholesterol, while shorter treatment durations had no effect on LDL cholesterol. The quantitative analysis did not provide data on long-term effects of Aronia on lipids. CONCLUSIONS: More long-term high-quality randomized controlled studies are needed to clarify if dietary supplementation with Aronia has beneficial effects on cardiometabolic diseases.

BACKGROUND: Subjects with type 2 diabetes (T2D) and their relatives (REL) carry an increased risk of cardiovascular disease (CVD). Low-grade inflammation, an independent risk factor for CVD, is modifiable by diet. Subjects with T2D show elevated postprandial inflammatory responses to fat-rich meals, while information on postprandial inflammation in REL is sparse. AIM: To clarify whether medium-chain saturated fatty acids (SFA) and monounsaturated fatty acids (MUFA) have differential acute effects on low-grade inflammation in REL compared to controls (CON). METHODS: In randomized order, 17 REL and 17 CON ingested two fat-rich meals, with 72 energy percent from MUFA and 79 energy percent from mainly medium-chain SFA, respectively. Plasma high sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), adiponectin, and leptin were measured at baseline, 15 min, 60 min, and 240 min postprandially. Muscle and adipose tissue biopsies were taken at baseline and 210 min after the test meal, and expression of selected genes was analyzed. RESULTS: Plasma IL-6 increased (p < 0.001) without difference between REL and CON and between the meals, whereas plasma adiponectin and plasma hs-CRP were unchanged during the 240 min observation period. Plasma leptin decreased slightly in response to medium-chain SFA in both groups, and to MUFA in REL. Several genes were differentially regulated in muscle and adipose tissue of REL and CON. CONCLUSIONS: MUFA and medium-chain SFA elicit similar postprandial circulating inflammatory responses in REL and CON. Medium-chain SFA seems more proinflammatory than MUFA, judged by the gene expression in muscle and adipose tissue of REL and CON.

Udgivelsesdato: 2008 Winter BACKGROUND: The influence of glucose and fatty acids on beta-cell function is well established whereas little is known about the role of amino acids (AAs). METHODS: Islets isolated from NMRI mice were incubated overnight. After preincubation, isolated islets as well as clonal INS-1E beta-cells were incubated for 60 min in a modified Krebs Ringer buffer containing glucose and AAs. RESULTS: At 16.7 mmol/l (mM) glucose, L-arginine, L-lysine, L-alanine, L-proline, L-leucine, and L-glutamine potentiated glucose-stimulated insulin secretion dose-dependently, while DL-homocysteine inhibited insulin secretion. Maximal insulin stimulation was obtained at 20 mM L-proline, L-lysine, L-alanine, L-arginine (islets: 2.5 to 6.7 fold increase; INS-1E cells: 1.6 to 2.2 fold increase). L-glutamine and L-leucine only increased glucose-stimulated (16.7 mM) insulin secretion (INS-1E cells: 1.5 and 1.3 fold, respectively) at an AA concentration of 20 mM. Homocysteine inhibited insulin secretion both at 5.6 mM and 16.7 mM glucose. At glucose levels ranging from 1.1 to 25 mM, the equimolar concentration of 10 mM, L-proline, L-lysine, L-arginine increased insulin secretion from mouse islets and INS-1E cells at all glucose levels applied, with a maximal effect obtained at 25 mM glucose. At a concentration of 10 mM, L-arginine and L-lysine had the highest insulinotropic potency among the AAs investigated. CONCLUSION: L-arginine, L-lysine, L-alanine, L-proline, L-leucine and L-glutamine acutely stimulate insulin secretion from mouse islets and INS-1E cells in a dose- and glucose-dependent manner, whereas DL-homocysteine inhibits insulin release.