“…The change was driven by hypercholesterolaemic participants.Jin et al (2014) | 9/6F 12/4F OW NAFLD | P, 4 | c: Fructose i: Glucose | 20 20 | Beverages | NSD: Bw | NSD: Liver fat | ↓ Adipose tissue IR index 9 NSD: FG, FI, HOMA‐IR | | ↓ VLDL NSD: TG | | Sugar type had no effect on body weight, liver fat or triglycerides. Adipose tissue IR and VLDL decreased with glucose vs. fructose |
Maersk et al (2012)* | 15/11F 16/11F 15/12F 14/6F OW/Obese | P, 24 | c1: SK milk c2: Water c3: ASSD i: SSSD | 0 0 0 18 | Beverages | NSD: Bw, BMI, BF, LBM | ↑ Liver fat ↑ VAT ↑ SKm fat (data available for 47 subjects) | NSD: FG, FI, HOMA‐IR; glucose and insulin responses (AUC) and derived indices of IR on OGTT | ↑ SBP (c1, c3) NSD: DBP | ↑ T‐c (vs c3) ↑ TG (vs c2 and c3) NSD: LDL‐c, HDL‐c, T‐c/HDL‐c ratio | ↑ FUA (data available for 47 subjects) | Consumption of SSSD increased triglycerides, uric acid and ectopic fat deposition with no effect on body weight, total body fat or glucose homeostasis |
Majid et al (2013) | 31 M 32 M GP | P, 4 | c: No drink i: Honey | 0 8 | Beverages | | | ↓ FG | | ↓ T‐c, LDL‐c, TG ↑ HDL‐c | | Honey consumption limited the rise in blood glucose and improved the blood lipid profile. Background diet and changes in body weight were not assessed. |
Mark et al (2014) | 35F 38F OW/OB | P, 4 | i: Fructose 10 c: Glucose 10 | 15 15 | Beverages | NSD: BW, BMI, WC | | NSD: FG, FI, HOMA‐IR; glucose and insulin responses and ISI on OGTT | | NSD: T‐c, LDL‐c, HDL‐c, TG | | |
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