An interventional study of Low fat diet and High fat diet in Pre-diabetes, sponsored by Laval University. Completed at 1 site in Canada. Open to participants aged 18 Years to 60 Years. Per ClinicalTrials.gov, last updated 2026-08-26.
Sponsored by Laval University · Not applicable, Interventional, and Prevention
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases, affecting 25% to 30% of the global population and nearly one third of the population in North America. NAFLD is defined as an excessive accumulation of lipids within hepatocytes in the absence of significant alcohol consumption or other causes of chronic liver disease. These patients usually present with hepatic steatosis observed on imaging studies and elevated liver enzymes with clinical features of insulin resistance (IR), including pre-diabetes, type 2 diabetes mellitus (T2DM), arterial hypertension, dyslipidemia, and visceral obesity. The minimum criterion for a histologic diagnosis of NAFLD is >5 percent steatotic hepatocytes in a liver tissue section. The exact mechanism for the development of NAFLD is unclear, although the current evidence indicates that it is likely a complex interplay among neurohormones, intestinal dysbiosis, nutrition, and genetics. IR plays a crucial role in NAFLD pathophysiology mainly by increasing adipocyte lipolysis, resulting in the circulation of more free fatty acids available for hepatic uptake and increasing hepatic de novo lipogenesis. There is yet no approved pharmacologic option for the treatment of NAFLD. Current international guidelines on NAFLD emphasize the importance of lifestyle modifications for all patients with NAFLD and recommend 7-10% of weight loss and a "healthy diet", without suggesting any particular diet. Recent data provide some support for the beneficial role of low carbohydrate (CHO)/high unsaturated fatty acid (both monounsaturated (MUFAs) and polyunsaturated (PUFAs)) dietary patterns for decreasing hepatic steatosis. This proposal addresses this important research gap by leading to advances regarding the impact of a short-term low CHO/high PUFAs/MUFAs dietary intervention on improving hepatic gene expression profiles and lipid composition in individuals with pre-diabetes. The proposed study is unique because all meals and foods will be provided to participants under carefully controlled isocaloric conditions to maintain a constant bodyweight with optimal energy and macronutrient intake control. The primary objective of the proposed research is to investigate how replacement of dietary CHOs by unsaturated fatty acids (both PUFAs and MUFAs) affects liver fat composition and liver transcriptomics in subjects with pre-diabetes.
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This study's enrollment of 6 is below the median of 60 across 645 interventional studies indexed under Glucose Intolerance.
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During 3 days, subjects eat a diet low in fat (percent of total caloric intake: 15.0% from proteins; 65.0% from carbohydrates; 20.0% from fat: 4.0% from saturated fat; 10.0% from monounsaturated fat; 6.0% from polyunsaturated fat
Other: Low fat diet · Other: High fat diet
During 3 days, subjects eat a diet high in fat (percent of total caloric intake: 15.0% from proteins; 45.0% from carbohydrates; 40.0% from fat: 8.0% from saturated fat; 22.0% from monounsaturated fat; 10.0% from polyunsaturated fat
Other: Low fat diet · Other: High fat diet
During 3 days, subjects eat a diet low in fat (percent of total caloric intake: 15.0% from proteins; 65.0% from carbohydrates; 20.0% from fat: 4.0% from saturated fat; 10.0% from monounsaturated fat; 6.0% from polyunsaturated fat
During 3 days, subjects eat a diet high in fat (percent of total caloric intake: 15.0% from proteins; 45.0% from carbohydrates; 40.0% from fat: 8.0% from saturated fat; 22.0% from monounsaturated fat; 10.0% from polyunsaturated fat
Change in the expression of key genes in lipid metabolism including LDL-receptor, acetyl-CoA acetyltransferase 2, apolipoprotein B, proproprotein convertase subtilisin/kexin type 9, microsomal triglyceride transfer protein
Time frame: At Day 3 and day 20 (at the end of the two 3-day diets)
Change in the expression of key genes in liver inflammation including C-reactive protein, Interleukin-6, Interleukin-15, cell adhesion molecules, E-selectin
Time frame: At Day 3 and day 20 (at the end of the two 3-day diets)
Change in the expression of key genes in hepatic fibrogenesis including transforming growth factor beta 1, a-smooth muscle actin, type-1 collagen, connective tissue growth factor
Time frame: At Day 3 and day 20 (at the end of the two 3-day diets)
Change in liver's key lipid pathways (lipidomics) including lysophosphatidylcholine, phosphatidylcholine, diglyceride.
Time frame: At Day 3 and day 20 (at the end of the two 3-day diets)
Identify bacteria strains involved in the control of blood glucose such as C elegans.
Time frame: At Day 3 and day 20 (at the end of the two 3-day diets)
This study is completed, as verified in Aug 2026. You cannot join it, but the record below documents what was studied.
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Laval University