Aims: Postprandial triglyceridaemia is a risk factor for cardiovascular disease (CVD). This study investigated the effects of steady‐state liraglutide 1.8 mg versus placebo on postprandial plasma lipid concentrations after 3 weeks of treatment in patients with type 2 diabetes mellitus (T2DM). Methods: In a cross‐over trial, patients with T2DM (n = 20, 18–75 years, BMI 18.5–40 kg/m ² ) were randomized to once‐daily subcutaneous liraglutide (weekly dose escalation from 0.6 to 1.8 mg) and placebo. After each 3‐week period, a standardized fat‐rich meal was provided, and the effects of liraglutide on triglyceride (primary endpoint AUC _0–8h ), apolipoprotein B48 , non‐esterified fatty acids, glycaemic responses and gastric emptying were assessed. ClinicalTrials.gov ID : NCT00993304 . Funding: Novo Nordisk A/S. Results: After 3 weeks, mean postprandial triglyceride (AUC _0–8h liraglutide/placebo treatment‐ratio 0.72, 95% CI [0.62–0.83], p = 0.0004) and apolipoprotein B48 (AUC _0–8h ratio 0.65 [0.58–0.73], p < 0.0001) significantly decreased with liraglutide 1.8 mg versus placebo, as did iAUC _0–8h and C _max (p < 0.001). No significant treatment differences were observed for non‐esterified fatty acids. Mean postprandial glucose and glucagon AUC _0–8h and C _max were significantly reduced with liraglutide versus placebo. Postprandial gastric emptying rate [assessed by paracetamol absorption (liquid phase) and the ¹³ C ‐octanoate breath test (solid phase)] displayed no treatment differences. Mean low‐density lipoprotein and total cholesterol decreased significantly with liraglutide versus placebo. Conclusions: Liraglutide treatment in patients with T2DM significantly reduced postprandial excursions of triglyceride and apolipoprotein B48 after a fat‐rich meal, independently of gastric emptying. Results indicate liraglutide's potential to reduce CVD risk via improvement of postprandial lipaemia.

The recommended amount and quality of protein in diets of diabetic patients are highly controversial. In order to provide evidence-based information, the Diabetes Nutrition Study Group (DNSG) used a grading procedure used for quality of evidence and strength of recommendations (GRADE). A protein intake of 10% to 20% of energy intake (E%) or about 0.8 to 1.3 g/kg body weight in people below 65 years of age, and 15% to 20% of E% in people above 65 years of age appeared safe in weight-stable conditions. There were no intervention studies addressing metabolic effects, mortality, or cardiovascular events over prolonged periods. Body weight is closely linked to metabolic control and high protein diets are often recommended. Weight-loss diets that include 23% to 32% of E% as protein for up to one year reduced blood pressure and body weight slightly but significantly more than lower protein diets, whereas blood lipids, fasting blood glucose, and HbA1c improved similarly with higher or lower protein intakes in participants with a glomerular filtration rate (GFR) >60 mL/min/1.73 m². Patients with a GFR <60 mL/min/1.73 m² did not show a faster decline of GFR or kidney function with protein intakes around 0.8 g/kg body weight as compared with lower intakes, thereby arguing against a restriction. The effects of protein intake on diabetic eye or nerve disease have not been reported. There are a number of studies that have compared different types of animal proteins (milk, chicken, beef, pork, and fish) or compared animal with plant protein in diabetic patients and have reported a greater reduction of serum cholesterol with plant protein. In summary, the suggested range of protein intake appears to be safe and can be adapted according to personal dietary preferences.

Limiting excessive postprandial glucose excursions is an important component of good overall glycemic control in diabetes mellitus. Pharmacokinetic studies have shown that insulin aspart, which is structurally identical to regular human insulin except for the replacement of a single proline amino acid with an aspartic acid residue, has a more physiologic time–action profile (i.e., reaches a higher peak and reaches that peak sooner) than regular human insulin. As expected with this improved pharmacokinetic profile, insulin aspart demonstrates a greater glucose-lowering effect compared with regular human insulin. Numerous randomized controlled trials and a meta-analysis have also demonstrated improved postprandial control with insulin aspart compared with regular human insulin in patients with type 1 or type 2 diabetes, as well as efficacy and safety in children, pregnant patients, hospitalized patients, and patients using continuous subcutaneous insulin infusion. Studies have demonstrated that step-wise addition of insulin aspart is a viable intensification option for patients with type 2 diabetes failing on basal insulin. Insulin aspart has shown a good safety profile, with no evidence of increased receptor binding, mitogenicity, stimulation of anti-insulin antibodies, or hypoglycemia compared with regular human insulin. In one meta-analysis, there was evidence of a lower rate of nocturnal hypoglycemia compared with regular human insulin and, in a trial that specifically included patients with a history of recurrent hypoglycemia, a significantly lower rate of severe hypoglycemic episodes. The next generation of insulin aspart (faster-acting insulin aspart) is being developed with a view to further improving on these pharmacokinetic/pharmacodynamic properties.

Since coffee may help to prevent the development of metabolic syndrome (MetS), we aimed to evaluate the short- and long-term effects of a coffee-based supplement on different features of diet-induced MetS. In this study, 24 Sprague Dawley rats were divided into control or nutraceuticals groups to receive a high-fat/high-fructose diet with or without a mixture of caffeic acid (30 mg/day), trigonelline (20 mg/day), and cafestol (1 mg/day) for 12 weeks. An additional 11 rats were assigned to an acute crossover study. In the chronic experiment, nutraceuticals did not alter body weight or glycemic control, but improved fed hyperinsulinemia (mean difference = 30.80 mU/L, p = 0.044) and homeostatic model assessment-insulin resistance (HOMA-IR) (mean difference = 15.29, p = 0.033), and plasma adiponectin levels (mean difference = −0.99 µg/mL, p = 0.048). The impact of nutraceuticals on post-prandial glycemia tended to be more pronounced after acute administration than at the end of the chronic study. Circulating (mean difference = 4.75 U/L, p = 0.014) and intrahepatocellular alanine transaminase activity was assessed by hyperpolarized-¹³C nuclear magnetic resonance NMR spectroscopy and found to be reduced by coffee nutraceuticals at endpoint. There was also a tendency towards lower liver triglyceride content and histological steatosis score in the intervention group. In conclusion, a mixture of coffee nutraceuticals improved insulin sensitivity and exhibited hepatoprotective effects in a rat model of MetS. Higher dosages with or without caffeine deserve to be studied in the future.

Diabetic dyslipidemia with elevated postprandial triglyceride (TG) responses is characteristic in type 2 diabetes (T2D). Diet and meal timing can modify postprandial lipemia (PPL). The impact of a pre-meal of whey proteins (WP) on lipid metabolism is unidentified. We determined whether a WP pre-meal prior to a fat-rich meal influences TG and apolipoprotein B-48 (ApoB-48) responses differentially in patients with and without T2D. Two matched groups of 12 subjects with and without T2D accomplished an acute, randomized, cross-over trial. A pre-meal of WP (20 g) or water (control) was consumed 15 min before a fat-rich meal (supplemented with 20 g WP in case of water pre-meal). Postprandial responses were examined during a 360-min period. A WP pre-meal significantly increased postprandial concentrations of insulin (P < 0.0001), glucagon (P < 0.0001) and glucose-dependent insulinotropic peptide (GIP) (P < 0.0001) in subjects with and without T2D. We detected no effects of the WP pre-meal on TG, ApoB-48, or non-esterified fatty acids (NEFA) responses to the fat-rich meal in either group. Paracetamol absorption i.e., gastric emptying was delayed by the WP pre-meal (P = 0.039). In conclusion, the WP pre-meal induced similar hormone and lipid responses in subjects with and without T2D. Thus, the WP pre-meal enhanced insulin, glucagon and GIP responses but did not influence lipid or glucose responses. In addition, we demonstrated that a WP pre-meal reduced gastric emptying in both groups.

Background: The global epidemic of type 2 diabetes (T2D) is a challenging health problem. Lifestyle changes, including nutrition therapy, areimportant for the prevention and management of T2D. Seaweeds contain several bioactive substances with potential health properties and may be a low-cost alternative functional food in the prevention of T2D. Objective: The aim of this study was to explore the preventive effects of dried Nordic seaweed species on diabetes in an animal model of T2D. Method: Fiftymale KK-Ay mice were randomly assigned to one of four diets: control diet (chow) or diets supplemented with Alaria esculenta (AE), Saccharina latissima (SL), or Palmaria palmata (PP). The effect of the interventions on the progression of T2D was monitored over 10 weeks and evaluated by circulating glucose, glycated hemoglobin (HbA1c), insulin, glucagon, and lipid levels. Results: The SL group had significantly lower bodyweight, lower HbA1c and insulin levels, as well as higher high density lipoprotein (HDL) cholesterol levels after the 10-week intervention than the control group. At the end of the study, the control group had significantly higher HbA1c (p < 0.001) than all of the seaweed groups. Conclusion: All seaweed groups improved HbA1C compared to control and Saccharinalatissima seaweed had concomitantly beneficial effects on glycemic control and lipid levels in KK-Ay diabetic mice.