Intermittent fasting may be an effective intervention to protect against age-related metabolic disturbances, although it is still controversial. Here, we investigated the effect of intermittent fasting on the deterioration of the metabolism and cognitive functions in rats with estrogen deficiency and its mechanism was also explored. Ovariectomized rats were infused with β-amyloid (25-35; Alzheimer's disease) or β-amyloid (35-25, Non-Alzheimer's disease; normal cognitive function) into the hippocampus. Each group was randomly divided into two sub-groups: one with intermittent fasting and the other fed ad libitum: Alzheimer's disease-ad libitum, Alzheimer's disease-intermittent fasting, Non-Alzheimer's disease-ad libitum, and Non-Alzheimer's disease-intermittent fasting. Rats in the intermittent fasting groups had a restriction of food consumption to a 3-h period every day. Each group included 10 rats and all rats fed a high-fat diet for four weeks. Interestingly, Alzheimer's disease increased tail skin temperature more than Non-Alzheimer's disease and intermittent fasting prevented the increase. Alzheimer's disease reduced bone mineral density in the spine and femur compared to the Non-Alzheimer's disease, whereas bone mineral density in the hip and leg was reduced by intermittent fasting. Fat mass only in the abdomen was decreased by intermittent fasting. Intermittent fasting decreased food intake without changing energy expenditure. Alzheimer's disease increased glucose oxidation, whereas intermittent fasting elevated fat oxidation as a fuel source. Alzheimer's disease and intermittent fasting deteriorated insulin resistance in the fasting state but intermittent fasting decreased serum glucose levels after oral glucose challenge by increasing insulin secretion. Alzheimer's disease deteriorated short and spatial memory function compared to the Non-Alzheimer's disease, whereas intermittent fasting prevented memory loss in comparison to ad libitum. Unexpectedly, cortisol levels were increased by Alzheimer's disease but decreased by intermittent fasting. Intermittent fasting improved dyslipidemia and liver damage index compared to ad libitum. Alzheimer's disease lowered low-density lipoprotein cholesterol and serum triglyceride levels compared to Non-Alzheimer's disease. In conclusion, Alzheimer's disease impaired not only cognitive function but also disturbed energy, glucose, lipid, and bone metabolism in ovariectomized rats. Intermittent fasting protected against the deterioration of these metabolic parameters, but it exacerbated bone mineral density loss and insulin resistance at fasting in Alzheimer's disease-induced estrogen-deficient rats. Impact statement Intermittent fasting was evaluated for its effects on cognitive function and metabolic disturbances in a rat model of menopause and Alzheimer's disease. Intermittent fasting decreased skin temperature and fat mass, and improved glucose tolerance with decreasing food intake. Intermittent fasting also prevented memory loss: short-term and special memory loss. ...

The first examples of room temperature ionic liquids, containing N-alkyl-N-vinyl-2-pyrrolidinonium (N-alkyl-N-vinyl-gamma-butyrolactam) cations in combination with bromide and tetrafluoroborate anions, have been synthesized and the spectroscopic and physical characteristics of this family of ionic liquids have been investigated for intended use as liquid electrolytes and green solvents.

Menopausal women are susceptible to osteoarthritis and memory impairment. We hypothesized that Alzheimer’s-like disease (AD) exacerbates osteoarthritis and that intermittent fasting(IMF) with a high-protein(H-P) diet would enhance memory function and relieve osteoarthritis symptoms in estrogen-deficient animals with surgically induced AD and osteoarthritis. The action mechanism was also explored. Ovariectomized Sprague-Dawley rats were fed high-fat(H-F) or H-P diets for two weeks, and then they had a hippocampal infusion of β-amyloid(25-35) for 4 weeks to induce AD and an injection of monoidoacetate(MIA) into the articular cartilage to induce osteoarthritis. Four groups had AD symptoms, whereas two groups had non-AD symptoms by hippocampal amyloid-β(35-25) infusion. All rats had an MIA injection into the articular cartilage of the left knee. IMF suppressed memory impairment in AD rats, especially those fed H-P diets. Compared to Non-AD, AD exacerbated osteoarthritis symptoms, including swelling, limping, slowed treadmill running speed, and uneven weight distribution in the left leg. The exacerbations were linked to increased inflammation and pain, but IMF and H-P lessened inflammation and pain-related symptoms. Lean body mass(LBM) also decreased with AD and IMF, but H-P protected against LBM loss. Histological examination of the knee joint revealed the degree of the cellular invasion into the middle zone, and the changes in the tidemark plateau were greatest in the AD-AL with H-F, while non-AD-IMF improved the cellular invasion to as much as non-AD-AL. H-P reduced the infiltration into the middle-zone of the knee and promoted collagen production. In conclusion, AD exacerbated the articular cartilage deterioration and memory impairment, and IMF with H-P alleviated the memory impairment and osteoarthritic symptoms by decreasing hippocampal amyloid-β deposition and proinflammatory cytokine expressions and by increasing LBM.