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We assessed the effect of a dietary pattern rich in unsaturated fatty acids (UFA), protein and fibers, without emphasizing energy restriction, on visceral adipose tissue (VAT) and cardiometabolic risk profile. Within the 36-months randomized controlled NutriAct trial, we randomly assigned 502 participants (50-80 years) to an intervention or control group (IG, CG). The dietary pattern of the IG includes high intake of mono-/polyunsaturated fatty acids (MUFA/PUFA 15-20% E/10-15% E), predominantly plant protein (15-25% E) and fiber (≥30 g/day). The CG followed usual care with intake of 30% E fat, 55% E carbohydrates and 15% E protein. Here, we analyzed VAT in a subgroup of 300 participants via MRI at baseline and after 12 months, and performed further metabolic phenotyping. A small but comparable BMI reduction was seen in both groups (mean difference IG vs. CG: -0.216 kg/m 2 [-0.477; 0.045], partial η 2 = 0.009, p = 0.105). VAT significantly decreased in the IG but remained unchanged in the CG (mean difference IG vs. CG: -0.162 L [-0.314; -0.011], partial η 2 = 0.015, p = 0.036). Change in VAT was mediated by an increase in PUFA intake (ß = -0.03, p = 0.005) and induced a decline in LDL cholesterol (ß = 0.11, p = 0.038). The NutriAct dietary pattern, particularly due to high PUFA content, effectively reduces VAT and cardiometabolic risk markers, independent of body weight loss.

The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) have their main physiological role in augmenting insulin secretion after their nutrient-induced secretion from the gut. A functioning entero-insular (gut-endocrine pancreas) axis is essential for the maintenance of a normal glucose tolerance. This is exemplified by the incretin effect (greater insulin secretory response to oral as compared to "isoglycaemic" intravenous glucose administration due to the secretion and action of incretin hormones). GIP and GLP-1 have additive effects on insulin secretion. Local production of GIP and/or GLP-1 in islet α-cells (instead of enteroendocrine K and L cells) has been observed, and its significance is still unclear. GLP-1 suppresses, and GIP increases glucagon secretion, both in a glucose-dependent manner. GIP plays a greater physiological role as an incretin. In type 2-diabetic patients, the incretin effect is reduced despite more or less normal secretion of GIP and GLP-1. While insulinotropic effects of GLP-1 are only slightly impaired in type 2 diabetes, GIP has lost much of its acute insulinotropic activity in type 2 diabetes, for largely unknown reasons. Besides their role in glucose homoeostasis, the incretin hormones GIP and GLP-1 have additional biological functions: GLP-1 at pharmacological concentrations reduces appetite, food intake, and-in the long run-body weight, and a similar role is evolving for GIP, at least in animal studies. Human studies, however, do not confirm these findings. GIP, but not GLP-1 increases triglyceride storage in white adipose tissue not only through stimulating insulin secretion, but also by interacting with regional blood vessels and GIP receptors. GIP, and to a lesser degree GLP-1, play a role in bone remodelling. GLP-1, but not GIP slows gastric emptying, which reduces post-meal glycaemic increments. For both GIP and GLP-1, beneficial effects on cardiovascular complications and neurodegenerative central nervous system (CNS) disorders have been observed, pointing to therapeutic potential over and above improving diabetes complications. The recent finding that GIP/GLP-1 receptor co-agonists like tirzepatide have superior efficacy compared to selective GLP-1 receptor agonists with respect to glycaemic control as well as body weight has renewed interest in GIP, which previously was thought to be without any therapeutic potential. One focus of this research is into the long-term interaction of GIP and GLP-1 receptor signalling. A GLP-1 receptor antagonist (exendin [9-39]) and, more recently, a GIP receptor agonist (GIP [3-30] NH 2 ) and, hopefully, longer-acting GIP receptor agonists for human use will be helpful tools to shed light on the open questions. A detailed knowledge of incretin physiology and pathophysiology will be a prerequisite for designing more effective incretin-based diabetes drugs., (© 2021 The Authors. Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd.)

Introduction: The mean age of the German population increased over the last years, which resulted in a higher prevalence of cardiovascular diseases, type 2 diabetes, cognitive impairment, sarcopenia and bone fractures. Current evidence indicates a preservation of human wellbeing in the elderly by a healthy diet, although the recommended macronutrient composition and quality remains unclear and needs further long-term investigation. In this context we investigate the effect of a specific dietary pattern on age-related disorders in a randomized controlled multi-center trial (RCT)., Methods: We assess the effect of a specific dietary pattern (NutriAct) with a high proportion of unsaturated fat, plant proteins and fibres (fat 35%-40% of total energy (%E) of which 15%E-20%E monounsaturated fatty acids (MUFA) and 10%E-15%E polyunsaturated fatty acids (PUFA), 15%E-25%E proteins, ≥30 g fibres per day and 35%E-45%E carbohydrates) on age-related impairment of health within a 36-months RCT conducted in the region of Berlin and Potsdam. 502 eligible men (n = 183) and women (n = 319), aged 50 to 80 years, with an increased risk to develop age-related diseases were randomly assigned to either an intervention group focusing on NutriAct dietary pattern or a control group focusing on usual care and dietary recommendations in accordance to the German Nutrition Society (DGE). In the intervention group, 21 nutrition counsellings as well as supplementation of rapeseed oil, oil cake and specific designed foods are used to achieve the intended NutriAct dietary pattern.The primary outcome is a composite endpoint of age-related disorders, including cardiovascular morbidity, decline of cognitive function as well as clinical features of sarcopenia. Secondary outcomes include diet-induced effects on quality of life, depression, frailty, cardiovascular function, bone density, fat distribution pattern, glucose, lipid and energy metabolism, as well as the identification of biomarkers linked with age-related disorders., Discussion: The findings of this trial will provide clinically relevant information regarding dietary effects on age-related impairment of health and will contribute to the definition of the optimal macronutrient composition in the context of healthy aging in the German population.

Aim: To compare high animal protein (AP) with high plant protein (PP) diets, differing in amino acid composition, in people with type 2 diabetes (T2DM)., Materials and Methods: We compared isocaloric diets containing 30% of energy either as AP or PP, using newly developed PP-enriched foods, both combined with 30% energy as fat and 40% as carbohydrates in 44 patients with T2DM over 6 weeks in a randomized parallel-group study. Insulin sensitivity was assessed by hyperinsulinaemic-euglycaemic clamps and cardiovascular variables were measured., Results: Uric acid decreased in both groups, but significantly more in the AP than the PP group. There were no significant differences in other variables, although glycated haemoglobin levels, diastolic blood pressure and fasting non-esterified fatty acid levels improved significantly in the PP but not in the AP group. Insulin sensitivity (M-value), C-reactive protein and fasting glucose improved significantly in the AP but not in the PP group. Total and LDL cholesterol levels and systolic blood pressure decreased significantly in both groups, and the urinary albumin excretion rate decreased from baseline in participants with microalbuminuria., Conclusions: Isocaloric diets high in AP or PP allow similar improvements in metabolism and cardiovascular risk factors in people with T2DM, indicating that the differences in amino acid composition do not affect the metabolic responses to the interventions., (© 2017 John Wiley & Sons Ltd.)

Background and aim: heart failure (HF) is associated with an increase of systemic and myocardial insulin resistance, decrease of metabolism of fatty acids (FA) and a shift toward glucose for ATP generation. The defects in FA oxidation, mitochondrial dysfunction and/or chronic activation of NP system are proposed as the possible triggers of development of metabolic disorder in HF; however the exact mechanisms of these disorders are largely unknown. Our goal was to investigate the alterations in PPAR and NP pathways in adipose tissue from heart failure patients using cellular in vitro models.Methods: in vitro adipodenic differentiation of previously characterized adipose (AD) and bone marrow (BM) derived MMSC from healthy donors (HD; n=4) and HF patients (n=4) was done. The stimulation of adipogenesis performed as widely described. Gene expression was measured by Q-PCR at days 0, 4, 8 and 11 after stimulation.Results: expression of genes responsible for energy metabolism, glucose utilization, and NP pathway during differentiation of MMSC from AD of HF and HD is demonstrated in Table 1. Dynamics of expression of these genes during differentiation of BMMSC were very similar.Conclusion: Our data indicate that in HF both, PPAR- and NP- dependent pathways as well as glucose utilization are altered in adipose of different origin. Results are in a good accordance with data from clinical and animal studies demonstrating that fetal gene program is reactivated in failing heart. We have proved here that adipose culture system from cardiovascular patients is a relatively easy available model to study mechanisms of cardiovascular metabolic disorders in vitro, and a good tool to test how adipose tissue responds at molecular levels to different physiological and pharmacological interventions.Table 1Healthy DonorHeart FailureControlDay 4Day 8Day 11ControlDay 4Day 8Day 11PPARg6+2,162+19*36+10*44+12*4,3+1,76,7+2,7(**)4,5+1,3(**)2,3+1,7(**)Pgc1a2,7+0,7229+58*68+25*34+10*3,1+118+2,3*/(**)7,9+2(**)2,1+1(**)a2p21,6+0,3210312+70541*72347+30338*36181+14212*5,6+3,239101+16053*20299+7330*537+376GLUT42,9+0,64,8+1,137+13*32+12*12+42,9+0,75,7+1,6(**)1,3+0,3(**)NPRA3,8+1,1312+46*91+29*47+15*3,2+0,536+10*/(**)9,2+4,9(**)2,2+1,3(**)NPRC3,3+1,239+11*20+2*12+1*6,7+1,131+5*8,2+1,4(**)3,6+1,8(**)*p<0,05 vs control; *p<0,05 vs control; (**)p<0,05 vs HD [ABSTRACT FROM AUTHOR]