Fructose prevents the development of hyperglycaemia in WBN/Kob diabetic fatty rats via maintaining high insulin levels. (22nd February 2022)

• Record Type: Journal Article
• Authors: Kaji, Noriyuki; Namekawa, Junichi; Takagi, Yoshiichi; Watanabe, Ayaka; Nemoto, Sayaka; Minami, Yukako; Katayanagi, Atusko; Kobayashi, Taiki; Asai, Fumitoshi
• Is Part Of: Clinical and experimental pharmacology and physiology. Volume 49:Number 5(2022)
• Page Start: 577
• Page End: 585
• Publication Date: 2022-02-22
• Subjects: fructose -- metabolic syndrome -- obesity -- pancreas -- rats -- type 2 diabetes mellitus; Clinical pharmacology -- Periodicals; Pharmacology, Experimental -- Periodicals; Physiology, Experimental -- Periodicals; Physiology, Pathological -- Periodicals; 615.1
• DOI: 10.1111/1440-1681.13629
• Languages: English
• ISSNs: 0305-1870

Abstract

Abstract: Fructose is considered to negatively affect type 2 diabetes mellitus (T2DM); however, there are contradictory reports. The present study aimed to elucidate the effects of fructose‐rich diet (FRD) on glucose metabolism of Wistar Bonn Kobori (WBN/Kob) fatty diabetic (WBKDF) rats, a spontaneous T2DM model, and Wistar rats. Wistar Bonn Kobori fatty diabetic and Wistar rats were fed either FRD or standard diet (STD) for 4 weeks. The food intake, body weight, plasma glucose and insulin were measured weekly. After the 4‐week challenge, rats were subjected to an intravenous glucose tolerance test (IVGTT). The liver and pancreas were used for histological analysis. The 4‐week challenge of FRD in Wistar rats did not cause hyperglycaemia, but increased insulin resistance (Homeostatic Model Assessment for Insulin Resistance [HOMA‐IR]). Feeding WBKDF rats with a FRD accelerated obesity, but prevented the onset of severe hyperglycaemia via maintaining high plasma insulin levels. Homeostatic Model Assessment for Insulin Resistance in WBKDF rats was not changed by FRD feeding. Intravenous glucose tolerance test revealed that FRD feeding in Wistar rats did not affect glucose tolerance, but slightly increased the plasma insulin level. In contrast, FRD feeding in WBKDF rats significantly reduced the glucose tolerance, but insulin response was not improved. Fructose‐rich diet feeding did not alter the β cell area in Wistar rats, but significantly increased it in WBKDF rats. In conclusion, FRD caused insulin resistance in Wistar rats, suggesting that fructose overconsumption is a risk factor for T2DM, whereas FRD inhibited severe hyperglycaemia by maintaining high insulin levels in WBKDF rats. Fructose may be a beneficial sugar for T2DM patients with severe obesity‐induced insulin resistance.