Circulating levels of five proglucagon-derived peptides in response to intravenous or oral glucose or lipids and to a mixed-meal in subjects with normal weight, overweight, and obesity.

AIMS: Proglucagon-derived peptides (PGDPs) secreted by the gut and pancreas play a major role in metabolism. We measured concentrations of five PGDPs in response to per os (PO) or intravenous (IV) glucose or lipid intake and a mixed meal test (MMT) consumed by subjects with normal weight, overweight or obesity. MATERIALS AND METHODS: GLP-1, oxyntomodulin and glicentin (gut-secreted PGDPs) and glucagon and MPGF (pancreas-secreted PGDPs) were assessed in: (a) 32 subjects receiving PO or IV glucose, lipids or water over 6 h, (b) 33 subjects with normal weight, overweight or obesity who consumed a MMT. RESULTS: (a) GLP-1, oxyntomodulin, glicentin and glucagon levels increase more profoundly and persistently after lipids PO (2.5  g/kg) than glucose PO (2.5  g/kg) or IV lipids (Intralipid/Liposyn II 20% at 0.35 ml/kg/h and Intralipid/Liposyn II 20% at 0.83  ml/kg/h for 6 h) or IV glucose (10% glucose at 3.6 ml/kg/h for 6 h). Oxyntomodulin and glicentin increased more than GLP-1 in response to lipids PO. MPGF levels decrease in response to glucose PO or IV indicating a shift towards preferential production of gut-secreted peptides. (b) Fasting and postprandial areas under the curve (AUCs) after MMT of GLP-1, MPGF and glucagon levels correlated positively with BMI. The fasting levels of glucagon and MPGF were elevated in obesity and remained elevated after the MMT. CONCLUSION: Circulating levels of PGDPs are differentially regulated by body weight, the type of macronutrients administered and the respective route of administration. Mechanistic studies are needed to define the exact mechanisms underlying this regulation. CLINICAL TRIAL REGISTRATION: Study 1 has the NCT01520454 and the NCT04888325 number in ClinicalTrials.gov. Study 2 has the number NCT01495754 in ClinicalTrials.gov.

Dietary sodium estimation methods: accuracy and limitations of old and new methods in individuals at high cardiovascular risk.

OBJECTIVE: Accurate and easy to use methods for dietary Na intake estimation in population level are lacking. We aimed at (i) estimating the mean Na intake in the group level using a variety of dietary methods (DM) and urinary methods (UM) and correlating them with 24-h urine collection (24UCol) and (ii) improving the accuracy of the existing DM. DESIGN: The most common DM (three 24-h dietary recalls (24DR) and FFQ) and UM (24UCol and spot urine collection using common equations) were applied. To improve the existing: (i) 24DR, discretionary Na was quantified using salt-related questions or adding extra 15 % in total Na intake and (ii) FFQ, food items rich in Na and salt-related questions were added in the standard questionnaire (NaFFQ). SETTING: National and Kapodistrian University of Athens, Greece. PARTICIPANTS: Totally, 122 high cardiovascular risk subjects (56·0 ± 12·6 years; 55·7 % males). RESULTS: Mean 24 h Na excretion (24UNa) was 2810 ± 1304 mg/d. Spot urine methods overestimated the 24UNa (bias range: -1781 to -492 mg) and were moderately correlated to 24UCol (r = 0·469-0·596, P ≤ 0·01). DM underestimated the 24UNa (bias range: 877 to 1212 mg) and were weakly correlated with 24UCol. The improved DM underestimated the 24UNa (bias range: 877 to 923 mg). The NaFFQ presented the smallest bias (-290 ± 1336 mg) and the strongest correlation with 24UCol (r = 0·497, P ≤ 0·01), but wide limits of agreement in Bland-Altman plots (-2909 mg; 2329 mg), like all the other methods did. CONCLUSIONS: The existing methods exhibit poor accuracy. Further improvement of the newly developed NaFFQ could be promising for more accurate estimation of mean dietary Na intake in epidemiological studies. Additional validation studies are needed.

Associations of dietary patterns with blood pressure and markers of subclinical arterial damage in adults with risk factors for CVD.

OBJECTIVE: Unhealthy diet is a modifiable risk factor leading to subclinical arterial damage (SAD), high BP and CVD. It was aimed to investigate the possible associations of dietary patterns (DPs) with SAD in adults having multiple CVD risk factors. DESIGN: Dietary intake was evaluated through two 24-h dietary recalls and principal component analysis was used to identify DPs. Oscillometry, applanation tonometry with pulse wave analysis and carotid ultrasound were used to assess peripheral and aortic BP, arterial stiffness and pressure wave reflections. SETTING: Laiko University Hospital, Athens, Greece. PARTICIPANTS: A total of 470 individuals (53·1 ± 14·2 years) with CVD risk factors were enrolled. RESULTS: A pattern characterised by increased consumption of whole-grain cereals, white meat and reduced consumption of sugar was positively associated with common carotid compliance (ß = 0·01, 95 % CI 0·00, 0·01), whereas a pattern high in refined cereals, red and processed meat was positively associated with brachial but not aortic systolic pressure (ß = 1·76, 95 % CI 0·11, 3·42) and mean arterial pressure (MAP) (ß = 1·18, 95 % CI 0·02, -2·38). Low consumption of low-fat dairy products, high consumption of full-fat cheese and butter was positively associated with MAP (ß = 0·97, 95 % CI 0·01, 1·95). Increased consumption of vegetables, fruits, fresh juices, fish and seafood was inversely associated with augmentation index (AIx) (ß = -1·01, 95 % CI -1·93, -0·09). CONCLUSION: Consumption of whole grains, white meat, fruits/vegetables, fish/seafood and avoidance of sugar was associated with improved SAD. Preference in refined grains, red/processed meat, high-fat cheese/butter and low intake of low-fat dairy products were associated with BP elevation. Future studies are needed to confirm the present findings.

Levels of dietary sodium intake: diverging associations with arterial stiffness and atheromatosis.

BACKGROUND: Recent epidemiological evidence suggests a J-shaped, rather than the classical linear, association between dietary sodium (Na) intake and cardiovascular (CV) disease. Numerous animal studies have shown the acceleration of atheromatosis in a low-salt diet but data in humans are scarce. Our aim was to test the hypothesis that in a cohort of patients who are CV-free, yet at increased CV risk, moderate Na intake is associated with lower prevalence of atheromatosis and arterial stiffening than those at very low Na intake. METHODS: Two 24-h dietary recalls were conducted to estimate Na intake. Atheromatosis (carotid and femoral plaques) was assessed by B-mode ultrasonography and arterial stiffness through tonometry (carotid-to-femoral pulse wave velocity, cf-PWV). RESULTS: In 901 individuals (age: 52.4 ± 13.8 years, 45.2% males), only females at 3rd and 4th quartile of total Na intake (derived from food and discretionary salt) had significantly lower probability to present femoral plaques than those at 1st quartile (751.0 ± 215.5 mg/day), even in the full-adjusted model [0.462(0.229-0.935) and p = 0.032 3rd quartile; 0.274(0.118-0.638) and p = 0.003 4th quartile]. On the contrary, male and female individuals at 3rd quartile had significantly higher probability to present arterial stiffness (PWV >10 m/s) than those at 1st quartile [1.991(1.047-3.785) and p = 0.036]. CONCLUSIONS: Overall, the present data suggest that very low Na intake is associated with: a) accelerated atheromatosis, verifying findings from animal models, and providing a possible explanation of the modern epidemiology and b) lower arterial stiffness, which is in line with previous human findings, therefore suggesting a diverging effect of Na in the two major arterial pathologies.

Current Data on Dietary Sodium, Arterial Structure and Function in Humans: A Systematic Review.

BACKGROUND: Subclinical arterial damage (SAD) (arteriosclerosis, arterial remodeling and atheromatosis) pre-exists decades before cardiovascular disease (CVD) onset. Worldwide, sodium (Na) intake is almost double international recommendations and has been linked with CVD and death, although in a J-shape manner. Studies regarding dietary Na and major types of SAD may provide pathophysiological insight into the association between Na and CVD. OBJECTIVES: Systematic review of data derived from observational and interventional studies in humans, investigating the association between dietary Na with (i) atheromatosis (arterial plaques); (ii) arteriosclerosis (various biomarkers of arterial stiffness); (iii) arterial remodeling (intima-media thickening and arterial lumen diameters). DATA SOURCES: Applying the PRISMA criteria, the PubMed and Scopus databases were used. RESULTS: 36 studies were included: 27 examining arteriosclerosis, four arteriosclerosis and arterial remodeling, three arterial remodeling, and two arterial remodeling and atheromatosis. CONCLUSIONS: (i) Although several studies exist, the evidence does not clearly support a clinically meaningful and direct (independent from blood pressure) effect of Na on arterial wall stiffening; (ii) data regarding the association of dietary Na with arterial remodeling are limited, mostly suggesting a positive trend between dietary Na and arterial hypertrophy but still inconclusive; (iii) as regards to atheromatosis, data are scarce and the available studies present high heterogeneity. Further state-of-the-art interventional studies must address the remaining controversies.