Foodprint 1.0: Physiological Acute Responses After Consumption of Confectionary Products
- Conditions
- Glucose, High BloodEndotoxemiaInflammatory ResponseOxidative Stress
- Interventions
- Other: chocolate bar version 1Other: control chocolate barOther: cream version 1Other: cream version 3Other: control snackOther: cream version 2Other: control cream
- Registration Number
- NCT03972878
- Lead Sponsor
- University of Parma
- Brief Summary
The composition of a food or a meal consumed plays an important role in the rate of postprandial endocrine and metabolic response, especially if high in fats, sugars and total energy content and a reduction in its entity is related to beneficial effects towards the prevention of several chronical diseases. The physiological postprandial response depends on several factors, both intrinsic, such as natural characteristic of food, and extrinsic, such as the way in which food is processed. This study aims at investigating postprandial hormonal, metabolic, oxidative stress, inflammation and endotoxaemia responses after the consumption of different commercial confectionary products made with different reformulation (ingredients and/or processing techniques).The principal scope of the study is to evaluate the impact of the reformulation of different snacks on postprandial responses. The investigators therefore designed a randomized controlled crossover trial, in which 15 healthy volunteers will consume different isocaloric confectionary products (snacks) and their related reformulation (total products number = 6) and a reference snack. Venous blood samples will be collected until 4-h after meal consumption. In order to evaluate postprandial hormonal, metabolic, oxidative stress, inflammation and endotoxaemia responses several markers will be evaluate:
* metabolic substrates: glucose; Triglycerides and NEFA;
* hormones: insulin; c-peptide; GLP-1, GIP, leptin, ghrelin, PYY;
* markers of inflammation: IL-6, IL-8, IL-10, IL-17, TNF-α, hsCRP, MCP-1;
* markers of oxidative stress and antioxidant capacity: GSH, FRAP;
* endotoxaemia: lipopolysaccharides (LPS).
These results will contribute to a detailed evaluation of the effects of reformulation on physiological events after meal consumption, leading to clarify if these variations in ingredients and/or processing techniques can modify postprandial responses, making them more similar to those originated from the reference snack.
- Detailed Description
Meal consumption, especially if high in fats, sugars and total energy content, leads to a transient rise in blood glucose and lipids. The extent of glycemic and lipidemic postprandial responses have been linked to the progression of cardiovascular and other chronic degenerative diseases, such as type 2 diabetes and Alzheimer through a substantial increase in oxidative stress, systemic inflammation, and endothelial dysfunction. In addition, some studies have shown that consuming a high fat meal is associated with a postprandial increase in plasma and serum endotoxin concentrations in humans. LPS, lipopolysaccharide, is considered a major predisposing factor for inflammation-associated diseases such as atherosclerosis, sepsis and obesity. Therefore, following a correct dietary model may be beneficial in order to limit postprandial excursion and to modulate hormonal responses involved in satiety.
The physiological postprandial response depends on several factors, both intrinsic, such as natural characteristic of food, and extrinsic, such as the way in which food is processed. Thus, the present study aims at evaluating if the reformulation of some commercial confectionery products can lead to an improvement of the nutritional profile, through a decrease of postprandial metabolic and hormonal, oxidative stress, inflammation and endotoxaemia responses in comparison with commercial confectionery products (snacks).
Recruitment & Eligibility
- Status
- COMPLETED
- Sex
- All
- Target Recruitment
- 13
- Healthy male and female adult subjects
- BMI > 30 kg/m2
- Metabolic disorders (diabetes, hypertension, dyslipidemia, glucidic intolerance)
- Chronic drug therapies for any pathologies (including psychiatric diseases)
- Dietary supplements affecting metabolism of glucose and lipid
- Celiac disease
- Pregnancy or lactation
- Lactose intolerance
- Food allergies
Study & Design
- Study Type
- INTERVENTIONAL
- Study Design
- CROSSOVER
- Arm && Interventions
Group Intervention Description chocolate bar version 1 chocolate bar version 1 control chocolate bar version 1 control chocolate bar control chocolate bar control chocolate bar cream version 1 cream version 1 control spreadable cream, version 1 cream version 3 cream version 3 control spreadable cream, version 3 control snack control snack control snack cream version 2 cream version 2 control spreadable cream, version 2 control cream control cream control spreadable cream
- Primary Outcome Measures
Name Time Method IAUC postprandial blood glucose 0 (fasting), 15, 30, 45, 60, 90, 120, 180, 240 minutes Incremental area under the curve of blood glucose postprandial response (IAUC)
- Secondary Outcome Measures
Name Time Method IAUC postprandial blood lipids triglycerides (TAG) and non esterified fatty acid (NEFA) 0 (fasting), 30, 60, 90, 120, 180, 240 minutes Incremental area under the curve for blood TAG and NEFA postprandial response (IAUC)
Postprandial response for blood LPS 0 (fasting), 60, 90, 120, 180, 240 minutes incremental blood LPS concentration at each timepoint of the curve
Postprandial response for blood hormones (insulin, c-peptide, ghrelin, Glucagon-like peptide 1 (GLP-1), Gastric inhibitory peptide (GIP), peptide YY (PYY), leptin) 0 (fasting), 15, 30, 45, 60, 90, 120, 180, 240 minutes incremental blood insulin concentration at each timepoint of the curve
Postprandial response for blood lipids triglycerides (TAG) and non esterified fatty acid (NEFA) 0 (fasting), 30, 60, 90, 120, 180, 240 minutes incremental blood TAG and NEFA concentration at each timepoint of the curve
IAUC postprandial blood inflammatory markers (IL-6, IL-8, IL-10, IL-17, TNF-α, hsCRP, MCP-1) 0 (fasting), 60, 90, 120, 180, 240 minutes Incremental area under the curve for blood inflammatory markers (IL-6, IL-8, IL-10, IL-17, TNF-α, hsCRP, MCP-1) postprandial response (IAUC)
Postprandial response for blood glucose 0 (fasting), 15, 30, 45, 60, 90, 120, 180, 240 minutes incremental blood glucose concentration at each timepoint of the curve
IAUC postprandial blood hormones (insulin, c-peptide, ghrelin, Glucagon-like peptide 1 (GLP-1), Gastric inhibitory peptide (GIP), peptide YY (PYY), leptin) 0 (fasting), 15, 30, 45, 60, 90, 120, 180, 240 minutes Incremental area under the curve for blood insulin postprandial response (IAUC)
Postprandial response for blood inflammatory markers (IL-6, IL-8, IL-10, IL-17, TNF-α, hsCRP, MCP-1) 0 (fasting), 60, 90, 120, 180, 240 minutes incremental blood inflammatory markers (IL-6, IL-8, IL-10, IL-17, TNF-α, hsCRP, MCP-1) concentration at each timepoint of the curve
IAUC postprandial blood oxidative stress related markers glutathione (GSH) and antioxidant capacity (Ferric ion reducing antioxidant power (FRAP)) 0 (fasting), 60, 90, 120, 180, 240 minutes Incremental area under the curve for blood oxidative stress related markers glutathione (GSH) and antioxidant capacity (Ferric ion reducing antioxidant power (FRAP))
IAUC postprandial blood endotoxemia (Lipopolysaccharides (LPS)) 0 (fasting), 60, 90, 120, 180, 240 minutes Incremental area under the curve for LPS
Postprandial response for blood oxidative stress related markers glutathione (GSH) and antioxidant capacity (Ferric ion reducing antioxidant power (FRAP)) 0 (fasting), 60, 90, 120, 180, 240 minutes incremental blood oxidative stress related markers glutathione (GSH) and antioxidant capacity (Ferric ion reducing antioxidant power (FRAP)) concentration at each timepoint of the curve
Trial Locations
- Locations (1)
University of Parma
🇮🇹Parma, Italy