Chlorogenic acids (CGA) are the most abundant polyphenols in coffee. Continuous consumption of CGA reduces body fat and body weight. Since energy metabolism and sleep are controlled by common regulatory factors, consumption of CGA might modulate sleep. Lack of sleep has been identified as a risk factor for obesity, hypertension and type 2 diabetes. The aim of this study was to determine the effects of ingesting CGA over 5 d on energy metabolism and sleep quality in humans. A total of nine healthy subjects (four male and five female) completed a placebo-controlled, double-blinded, cross-over intervention study. Subjects consumed a test beverage containing 0 or 600 mg of CGA for 5 d. On the fifth night, subjects stayed in a whole-room metabolic chamber to measure energy metabolism; sleep was evaluated using polysomnographic recording. It was found that CGA shortened sleep latency (9 (sem 2) v. 16 (sem 4) min, P<0·05) compared with the control, whereas no effect on sleep architecture, such as slow-wave sleep, rapid eye movement or waking after sleep onset, was observed. Indirect calorimetry revealed that consumption of CGA increased fat oxidation (510 (sem 84) kJ/8 h (122 (sem 20) kcal/8 h) v. 331 (sem 79) kJ/8 h (81 (sem 19) kcal/8 h), P<0·05) but did not affect energy expenditure during sleep. Consumption of CGA enhanced parasympathetic activity assessed from heart-rate variability during sleep (999 (sem 77) v. 919 (sem 54), P<0·05). A period of 5-d CGA consumption significantly increased fat oxidation during sleep, suggesting that beverages containing CGA may be beneficial to reduce body fat and prevent obesity. Consumption of CGA shortened sleep latency and did not adversely affect sleep quality.
Summary Energy metabolism and substrate oxidation during sleep correlate with sleep stage, suggesting that energy metabolism affects sleep architecture or vice versa. The aim of the present study was to examine whether changes in energy metabolism during sleep, induced by a high-carbohydrate or high-fat meal for dinner, affect sleep architecture. Ten healthy males participated in this study, sleeping 3 nonconsecutive nights in a whole-room calorimeter. The first night was scheduled as an adaptation to the experimental environment. The other 2 nights were experimental calorimetry in a balanced cross-over design with intrasubject comparisons. In each session, subjects comsumed a high carbohydrate (HCD: PFC510 : 10 : 80) or high fat (HFD: PFC510 : 78 : 12) meal at 2000 h and slept with a polysomnographic recording in a metabolic chamber for indirect calorimetry (0000 h to 0800 h). Slow wave sleep was decreased during the first sleep cycle and not changed during the second or third sleep cycle under HCD conditions compared with those of HFD. Energy expenditure was not affected by dietary condition but substrate oxidation reflected differences in dietary composition of the dinner during the first and second sleep cycle. The present study suggested the possibility that substrate availability during sleep affects substrate oxidation during sleep, and affects sleep architecture during the first sleep cycle.
Consumption of milk fat globule membrane (MFGM) in combination with habitual exercise suppresses age-associated muscle loss. The effects of high dose MFGM, however, are not known. A double-blind, randomized controlled trial with parallel group design was conducted to evaluate the safety of consuming high dose MFGM tablets. The subjects were 32 healthy adult men and women. Subjects were given 5 times the recommended daily intake of the tablets containing 6.5 g of MFGM or whole milk powder for 4 weeks. Stomach discomfort and diarrhea were observed; however, these symptoms were transitory and slight and were not related to consumption of the test tablets. In addition, there were no clinically significant changes in anthropometric measurements or blood tests. Total degree of safety assessed by the physicians of all subjects was “safe.” These findings suggest that consumption of the tablets containing 6.5 g MFGM for 4 weeks is safe for healthy adults.
Effects of meal frequency on blood glucose levels and glucose metabolism were evaluated over 3 days in adult males with normal glucose tolerance (NGT, n = 9) or impaired fasting glucose (IFG, n = 9) in a randomized, crossover comparison study. Subjects were provided with an isocaloric diet 3 times daily (3M) or 9 times daily (9M). Blood glucose was monitored on Day 3 using a continuous glucose monitoring system, and subjects underwent a 75-g oral glucose tolerance test (OGTT) on Day 4. Daytime maximum blood glucose, glucose range, duration of glucose ≥180 mg/dL, and nighttime maximum glucose were significantly lower in the NGT/9M condition than in the NGT/3M condition. Similar findings were observed in the IFG subjects, with a lower daytime and nighttime maximum glucose and glucose range, and a significantly higher daytime minimum glucose in the 9M condition than in the 3M condition. The OGTT results did not differ significantly between NGT/3M and NGT/9M conditions. In contrast, the incremental area under the curve tended to be lower and the maximum plasma glucose concentration was significantly lower in the IFG/9M condition than in the IFG/3M condition. In IFG subjects, the 9M condition significantly improved glucose metabolism compared with the 3M condition. Higher meal frequency may increase glucagon-like peptide 1 secretion and improve insulin secretion.
When 56 selected environmental chemicals were tested for the androgenic activity to Yeast Two-hybrid and reporter gene assay in the presence of 5α-dihydrotestosterone (DHT), the activity was inhibited by some of the chemicals including N-nitrosodiphenylamine (NDPA), a novel anti-androgenic compound, and one of suspected carcinogenic N-nitrosocompounds (NOCs) commonly used as material of rubber and plastic goods. We further examined 15 NOCs for anti-androgenic activity, and found that N-nitrosodibenzylamine (NDBzA) and Nnitrosodicyclohexylamine (NDCHA) as well as NDPA inhibited the activity of DHT in a dose-dependent manner. These compounds showed the competitive binding to androgen receptor (AR) against DHT and decreased the level of AR protein. Furthermore, 3 NOCs down-regulated the prostate specific antigen (PSA) at the transcriptional level in LNCaP cells. These results suggest that some NOCs antagonized the androgenic effect of DHT in the same manner as the synthetic anti-androgen, flutamide (F).
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