Dietary curcumin restores insulin homeostasis in diet-induced obese aged mice

Cardiovascular disease (CVD) is the main cause of death in peritoneal dialysis (PD) patients, a situation that can be explained by a combination of traditional and nontraditional risk factors for CVD in these patients. Glucose and insulin homeostasis are altered in chronic kidney disease (CKD) patients even in the early stages of CKD, leading to insulin resistance by various pathways. Several factors have been implicated in the pathogenesis of insulin resistance, including anemia, dyslipidemia, uremia, malnutrition, excess of parathyroid hormone, vitamin D deficiency, metabolic acidosis, and increase in plasma free fatty acids and proinflammatory cytokines. Insulin resistance and dyslipidemia are observed and increase with the progression of CKD, playing an important role in the pathogenesis of hypertension and atherosclerosis. Particularly in PD patients, exposure to glucose from dialysis fluid accentuates the foregoing metabolic abnormalities. In conclusion, insulin resistance and altered glucose metabolism are frequently observed in CKD, and although dialysis partly corrects those disturbances, the use of glucose PD solutions intensifies a series of harmful metabolic consequences. New therapeutic measures aimed at reducing metabolic disorders are urgently needed and perhaps will improve PD patient survival.

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Supplementation with vitamin D and insulin homeostasis in healthy overweight and obese adults: A randomized clinical trial

Obesity Research & Clinical Practice ◽

10.1016/j.orcp.2021.03.004 ◽

2021 ◽

Author(s):

Seyed Alireza Ebadi ◽

Laleh Sharifi ◽

Elaheh Rashidi ◽

Seyed Shayan Ebadi ◽

Shayesteh Khalili ◽

...

Keyword(s):

Clinical Trial ◽

Vitamin D ◽

Randomized Clinical Trial ◽

Obese Adults ◽

Insulin Homeostasis

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γ‐Oryzanol improves exercise endurance and muscle strength by upregulating PPARδ and ERRγ activity in aged mice

Molecular Nutrition & Food Research ◽

10.1002/mnfr.202000652 ◽

2021 ◽

pp. 2000652

Author(s):

Jisong Ahn ◽

Hyo Jeong Son ◽

Hyo Deok Seo ◽

Tae Youl Ha ◽

Jiyun Ahn ◽

...

Keyword(s):

Muscle Strength ◽

Aged Mice ◽

Exercise Endurance

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Bcl-2-dependent autophagy disruption during aging impairs amino acid utilization that is restored by hochuekkito

npj Aging and Mechanisms of Disease ◽

10.1038/s41514-021-00065-8 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Miwa Nahata ◽

Sachiko Mogami ◽

Hitomi Sekine ◽

Seiichi Iizuka ◽

Naoto Okubo ◽

...

Keyword(s):

Amino Acid ◽

Energy Homeostasis ◽

Mitochondrial Dynamics ◽

Negative Regulator ◽

Aged Mice ◽

Glucose Levels ◽

Therapeutic Benefits ◽

Age Related ◽

Daily Food ◽

Young Mice

AbstractChronic undernutrition contributes to the increase in frailty observed among elderly adults, which is a pressing issue in the sector of health care for older people worldwide. Autophagy, an intracellular recycling system, is closely associated with age-related pathologies. Therefore, decreased autophagy in aging could be involved in the disruption of energy homeostasis that occurs during undernutrition; however, the physiological mechanisms underlying this process remain unknown. Here, we showed that 70% daily food restriction (FR) induced fatal hypoglycemia in 23–26-month-old (aged) mice, which exhibited significantly lower hepatic autophagy than 9-week-old (young) mice. The liver expressions of Bcl-2, an autophagy-negative regulator, and Beclin1–Bcl-2 binding, were increased in aged mice compared with young mice. The autophagy inducer Tat-Beclin1 D11, not the mTOR inhibitor rapamycin, decreased the plasma levels of the glucogenic amino acid and restored the blood glucose levels in aged FR mice. Decreased liver gluconeogenesis, body temperature, physical activity, amino acid metabolism, and hepatic mitochondrial dynamics were observed in the aged FR mice. These changes were restored by treatment with hochuekkito that is a herbal formula containing several autophagy-activating ingredients. Our results indicate that Bcl-2 upregulation in the liver during the aging process disturbs autophagy activation, which increases the vulnerability to undernutrition. The promotion of liver autophagy may offer clinical therapeutic benefits to frail elderly patients.

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