Saccharin Increases Fasting Blood Glucose but Not Liver Insulin Resistance in Comparison to a High Fructose-Fed Rat Model

Autor: Ehud Grossman, Iris Barshack, Ariel Bier, Avshalom Leibowitz, Mayan Gilboa, Edna Peleg
Rok vydání: 2018
Předmět:
0301 basic medicine
Blood Glucose
Male
medicine.medical_specialty
Non-Nutritive Sweeteners
saccharin
medicine.medical_treatment
lcsh:TX341-641
Fructose
Carbohydrate metabolism
Weight Gain
Article
metabolic syndrome
fatty liver
fructose
insulin resistance
Rats
Sprague-Dawley
03 medical and health sciences
chemistry.chemical_compound
Insulin resistance
Non-alcoholic Fatty Liver Disease
Internal medicine
Insulin Secretion
medicine
Animals
Insulin
Glycolysis
Triglycerides
Nutrition and Dietetics
Chemistry
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
Fatty liver
medicine.disease
030104 developmental biology
Endocrinology
Gene Expression Regulation
Liver
Hyperglycemia
Homeostatic model assessment
Metabolic syndrome
Diet
Carbohydrate Loading
lcsh:Nutrition. Foods and food supply
Biomarkers
Food Science
Zdroj: Nutrients
Nutrients; Volume 10; Issue 3; Pages: 341
Nutrients, Vol 10, Iss 3, p 341 (2018)
ISSN: 2072-6643
Popis: Recent data indicate that artificial sweeteners (AS) may have deleterious effects on glucose metabolism. The purpose of this study was to compare the effects of AS and the effects of a high fructose diet (HFrD) on glucose metabolism and insulin resistance (IR) in Sprague-Dawley (SD) rats. SD rats were fed either regular chow, chow with saccharin (Sac) (0.1 mg/mL) placed in their water, or HFrD for seven weeks. Glucose, insulin, and triglycerides (Tg) levels were measured upon completion. A homeostatic model assessment (HOMA)-IR index was used to determine insulin resistance. The liver was stained to detect signs of a fatty liver. Hepatic mRNA expression of glucose metabolism regulation genes, Srepb-1c (sterol regulatory element binding protein) and ChREB (α & β) (carbohydrate response element binding protein), as well as other glycolytic and lipogenic genes including glucose-6-phosphatase (G6pc), were considered IR markers. Both HFrD and Sac significantly increased fasting blood glucose levels compare to the control (140 ± 5 and 137 ± 6 vs. 118 ± 3 mg/dL, respectively, p < 0.05). However, only HFrD increased insulin secretion (0.99 ± 0.12 vs. 0.7 ± 0.1 and 0.6 ± 0.1 ug/L), Tg levels (420 ± 43 vs. 152 ± 20 and 127 ± 13 mg/dL), and the HOMA-IR index (3.4 ± 0.4 vs. 2.3 ± 0.36 and 2.13 ± 0.3) (HFrD vs. control and sac, p < 0.05). Fatty liver changes were only observed in HFrD fed rats. The expression of ChREB β, Srepb-1c, and G6pc mRNA were only significantly elevated (between 2–10 times folds, p < 0.05) in HFrD fed rats. Sac may increase fasting blood glucose but has no effect on liver insulin resistance.
Databáze: OpenAIRE
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