Accurate dietary analysis of energy, nutrient intake, and meal timing in human studies using traditional dietary assessment methods (e.g., food records) is challenging and time-consuming. The widespread use of smartphones, tablets, and nutrition applications (apps) can overcome some of these problems. The objective of this study was to evaluate the validity of an FDDB smartphone app and food database compared with PRODI^®—a professional platform for nutritional counselling using the German Nutrient Database. Dietary records were collected from 10 subjects participating in the crossover intermittent fasting trial for 2 weeks at baseline and during the eating timeframe of 8 h (early or late in the course of the day). The FDDB app and database enabled a quicker and less sophisticated analysis of food composition and timing than the PRODI^® software. Good agreement between the methods was found for energy and macronutrient intakes, while the FDDB data on most micronutrients and saturated/unsaturated fat intake were unreliable. In contrast to PRODI^®, FDDB provided effective assessment of timely compliance, making it a promising tool for chrononutritional studies. Thus, the FDDB app is comparable to the traditional PRODI^® dietary assessment method, and can be effectively used in human dietary trials and medical practice for specific goals.

Time-restricted eating (TRE) is a promising strategy to improve metabolic outcomes. However, it remains unclear whether TRE has cardiometabolic benefits in an isocaloric setting and whether its effects depend on the eating timing. We conducted a randomized crossover trial in 31 women with overweight or obesity to directly compare the effects of a 2-week early TRE (eTRE; eating from 8:00 to 16:00) and a 2-week late TRE (lTRE; eating from 13:00 to 21:00) on insulin sensitivity, cardiometabolic risk factors, and the internal circadian phase. During the restricted 8-hour eating period, participants were asked to consume their habitual food quality and quantity. Insulin sensitivity did not differ between (−0.07; 95% CI, −0.77 to 0.62; P = 0.60) or within (eTRE: 0.31; 95% CI, −0.14 to 0.76; P = 0.11; lTRE: 0.19; 95% CI, −0.22 to 0.60; P = 0.25) interventions. Twenty-four–hour glucose, lipid, inflammatory, and oxidative stress markers showed no clinically meaningful between- or within-intervention differences. Participants demonstrated high timely adherence (eTRE, 96.5%; lTRE, 97.7%), unchanged dietary composition and physical activity, minor daily calorie deficit (eTRE, −167 kilocalories/day), and weight loss (eTRE, −1.08 kilograms; lTRE, −0.44 kilograms). In lTRE, the circadian phase in blood monocytes (24 minutes; 95% CI, −5 to 54 minutes; P = 0.10) and sleep midpoint (15 minutes; 95% CI, 7 to 23 minutes; P < 0.001) occurred later compared with eTRE. Overall, in an intended isocaloric setting, neither eTRE nor lTRE improves insulin sensitivity or other cardiometabolic traits, despite a shift of internal circadian clocks.

Background: The dysfunction of energy metabolism in white adipose tissue (WAT) induces adiposity. Obesogenic diets that are high in saturated fat disturb nutrient metabolism in adipocytes. This study investigated the effect of an isocaloric high-fat diet without the confounding effects of weight gain on the gene expression of fatty acid and carbohydrate transport and metabolism and its genetic inheritance in subcutaneous (s.c.) WAT of healthy human twins. Methods: Forty-six healthy pairs of twins (34 monozygotic, 12 dizygotic) received an isocaloric carbohydrate-rich diet (55% carbohydrates, 30% fat, 15% protein; LF) for 6 weeks followed by an isocaloric diet rich in saturated fat (40% carbohydrates, 45% fat, 15% protein; HF) for another 6 weeks. Results: Gene expression analysis of s.c. WAT revealed that fatty acid transport was reduced after one week of the HF diet, which persisted throughout the study and was not inherited, whereas intracellular metabolism was decreased after six weeks and inherited. An increased inherited gene expression of fructose transport was observed after one and six weeks, potentially leading to increased de novo lipogenesis. Conclusion: An isocaloric dietary increase of fat induced a tightly orchestrated, partially inherited network of genes responsible for fatty acid and carbohydrate transport and metabolism in human s.c. WAT.

Background/Objectives: Emerging data support evidence of the essential role of glucagon for lipid metabolism. However, data on the role of dietary fat intake for glucagon secretion is limited. This analysis investigated whether altering nutritional fat intake affects glucagon levels in healthy subjects. Methods: A total of 92 twins (age: 31 ± 14 years, BMI: 23 ± 3 kg/m²) consumed two 6-week diets: first a low-fat, high-carbohydrate diet (LFD) followed by an isocaloric high-fat, low-carbohydrate diet (HFD). In total, 24 twins (age: 39 ± 15 years, BMI: 24 ± 2 kg/m²) continued with a high-protein diet (HPD). Clinical investigations were performed after 6 weeks of the LFD, after 1 and 6 weeks of the HFD and after 6 weeks of the HPD. Results: The LFD caused a significant decrease in fasting glucagon (−27%, p < 0.001) compared to baseline. After 6 weeks of the HFD, glucagon increased (117%, p < 0.001 vs. LFD), while free fatty acids decreased. Six weeks of the HPD further increased glucagon levels (72%, p = 0.502 vs. HFD), although fasting amino acid levels remained constant. Fasting insulin and HOMA-IR moderately increased after one week of the HFD, while six weeks of the HPD significantly decreased both. The fasting glucagon-to-insulin ratio decreased during the LFD (p < 0.001) but increased after the HFD (p < 0.001) and even further increased after the HPD (p = 0.018). Liver fat, triglycerides and blood glucose did not increase during the HFD. The heritability of glucagon levels was 45% with the LFD. Conclusions: An HFD increases glucagon levels and the glucagon-to-insulin ratio under isocaloric conditions compared to an LFD in healthy lean subjects. This rise in glucagon may represent a metabolic response to prevent hepatic steatosis, as glucagon increases have been previously shown to induce hepatic fat oxidation.

To investigate the impact of diabetes duration and different nutrient profiles on type 2 diabetes remission (T2DR) in response to very low-calorie diets (VLCDs). Participants with a BMI > 27 kg/m² and diabetes duration of ≤ 4 years or ≥ 8 years were studied before and after a VLCD (600-800 kcal/day) for three months, including discontinuation of antidiabetic medication. Individuals were randomly assigned to one of two VLCDs with slightly different macronutrient composition. T2DR, defined as plasma fasting glucose < 126 mg/dl, was achieved in 34 of 47 participants (72%). Despite similar weight loss of subjects with short and long diabetes duration (-15.2 ± 5.8 kg vs. -13.9 ± 4.8 kg; p = 0.473), subjects with long diabetes duration had a 32% lower remission rate (82% vs. 50%; p = 0.027).T2DR was found to be higher with the high-fiber, high-protein, and low-carb, low-fat formula diet (91% vs. 56%; p = 0.008). Individuals that achieved T2DR had significantly lower fasting plasma glucose and higher C-peptide levels at baseline. Fasting plasma glucose, C-peptide levels, diabetes duration, and used macronutrient profile emerged as important factors for the achievement of T2DR, although a considerable remission is still possible after long duration of type 2 diabetes.