Sustained Effects of a Non-glucidic Nutrient Preload on Glucose Tolerance in Type 2 Diabetes

Sustained Effects of a Non-glucidic Nutrient Preload on Glucose Tolerance in Type 2 Diabetes

The investigators aimed at evaluating the effects of a small non-glucidic nutrient preload on plasma glucose, insulin, C-peptide, glucagon-like peptide-1, and glucose-dependent insulinotropic polypeptide concentrations after the meal consumption and for 300 min after a 75 g glucose ingestion in diet-controlled type 2 diabetic patients.

As supported by experimental and clinical data, oral carbohydrate tolerance is influenced by the coingestion of nutrients through multiple mechanisms. The ingestion itself, the contact with the gastric mucosa, the arrival into the intestine and the subsequent digestion are known to produce neural reflexes, hormonal responses and plasma substrates gradients which, by modulating gastric emptying, insulin secretion and insulin clearance participate in the regulation of postprandial glycaemia. The size of this effect is influenced by a number of factors: the specific nutrient chemical characteristics (fat vs protein and composition) and their physical properties (solid vs liquid), the timing (pre-load vs coingestion) and finally the individual glucose tolerance status. The effect on 5 h glucose excursions of a combination of protein and fat given before carbohydrate is still unknown.

Inclusion Criteria:

• Diet-controlled type 2 diabetic patients
• Subjects ≥ 18 and ≤65 years of age
• Lean, Overweight or Obese (BMI: 18 to 35 kg/m2)
• Normal liver and kidney function
• Normal thyroid function
• Read and understood the informed consent form and signed it voluntarily

Exclusion Criteria:

• Liver, heart, kidney, lung, infectious, neurological, psychiatric, immunological or neoplastic diseases.
• Type 1 or insulin treated diabetes.
• Pregnancy or lactation
• Illicit drug abuse or alcoholism
• Subjects taking anoretic drugs
• Subjects on steroid treatment
• Subjects after bariatric surgery.