Research Article Details
Article ID: | A52196 |
PMID: | 30212233 |
Source: | Chronobiol Int |
Title: | Timing of food intake is more potent than habitual voluntary exercise to prevent diet-induced obesity in mice. |
Abstract: | Inappropriate eating habits such as skipping breakfast and eating late at night are associated with risk for abnormal weight-gain and adiposity. We previously reported that time-imposed feeding during the daytime (inactive phase) induces obesity and metabolic disorders accompanied by physical inactivity in mice. The present study compares metabolic changes induced in mice by time-imposed feeding under voluntary wheel-running (RW) and sedentary (SED) conditions to determine the effects of voluntary wheel-running activity on obesity induced in mice by feeding at inappropriate times. Mice were individually housed in cages with or without running-wheels. We compared food consumption, core body temperature, hormonal and metabolic variables in the blood, lipid accumulation in the liver, circadian expression of clock and metabolic genes in peripheral tissues, and gains in body weight between mice allowed access to food only during the sleep phase (daytime feeding; DF) or only during the active phase (nighttime feeding; NF) under SED or RW conditions. Only a high-fat high-sucrose diet was available to the mice throughout restricted feeding. Nocturnal activity was maintained in both NF and DF mice under RW conditions, but significantly suppressed during the latter half of the dark phase in DF mice. Nocturnal fluctuations in core body temperature were maintained in DF and NF mice under both SED and RW conditions, although DF attenuated the day-night amplitude more under SED, than RW conditions. The degrees of DF-induced increases in body weight gain, food efficiency, adipose tissue mass, lipogenic gene expression in metabolic tissues, and hepatic lipid accumulation were essentially identical between SED and RW conditions. Daytime feeding also induced hyperinsulinemia and hyperleptinemia under both SED and RW conditions, although DF-induced hyperleptinemia was slightly attenuated by wheel-running. The temporal expression of circadian clock genes became synchronized to feeding cycles in the liver but not in the skeletal muscle of mice under both SED and RW conditions. Chronic voluntary exercise on running-wheels minimally affected obesity and adiposity in mice caused by daily feeding at unusual times. The timing of food intake might be more important than physical exercise for preventing metabolic disorders. Abbreviations: ANOVA: analysis of variance; DF: daytime feeding; FFA: free fatty acid; GLP-1: glucagon-like peptide-1; HOMA-IR: homeostasis model assessment of insulin resistance; NEAT: non-exercise activity thermogenesis; NF: nighttime feeding; RF: restricted feeding; RW: running-wheel; SCN: suprachiasmatic nucleus; SE: standard error of the mean; SED: sedentary; SPA: spontaneous physical activity; T-Cho: total cholesterol; TG: triglyceride; WAT: white adipose tissues. |
DOI: | 10.1080/07420528.2018.1516672 |

Strategy ID | Therapy Strategy | Synonyms | Therapy Targets | Therapy Drugs | |
---|---|---|---|---|---|
S08 | Lifestyle measures | Lifestyle intervention; weight loss; diet adaptation; dietary interventions; lifestyle modifications; Exercise | -- | -- | Details |
S01 | Improve insulin resistance | insulin sensitizer; insulin resistance; glucose tolerance | Biguanide: increases 5-AMP activated protein kinase signaling; SGLT-2 inhibitor; Thiazalidinedione: selective PPAR-γ agonists; GLP-1 agonist | Metformin; Empagliflozin; Canagliflozin; Rosiglitazone; Pioglitazone; Liraglutide | Details |
Target ID | Target Name | GENE | Action | Class | UniProtKB ID | Entry Name | |
---|---|---|---|---|---|---|---|
T10 | Caspase-1 | CASP1 | inhibitor | Enzyme | P29466 | CASP1_HUMAN | Details |
T18 | Acetyl-CoA carboxylase 1 | ACACA | inhibitor | Enzyme | Q13085 | ACACA_HUMAN | Details |
T20 | Fatty acid synthase | FASN | inhibitor | Enzyme | P49327 | FAS_HUMAN | Details |
T06 | Glucagon-like peptide 1 receptor | GLP1R | agonist | GPCR | P43220 | GLP1R_HUMAN | Details |
Diseases ID | DO ID | Disease Name | Definition | Class | |
---|---|---|---|---|---|
I05 | 9352 | Type 2 diabetes mellitus | A diabetes that is characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both. A diabetes mellitus that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. http://en.wikipedia.org/wiki/Diabetes, http://en.wikipedia.org/wiki/Diabetes_mellitus_type_2 | disease of metabolism/inherited metabolic disorder/ carbohydrate metabolic disorder/glucose metabolism disease/diabetes/ diabetes mellitus | Details |
I14 | 9970 | Obesity | An overnutrition that is characterized by excess body fat, traditionally defined as an elevated ratio of weight to height (specifically 30 kilograms per meter squared), has_material_basis_in a multifactorial etiology related to excess nutrition intake, decreased caloric utilization, and genetic susceptibility, and possibly medications and certain disorders of metabolism, endocrine function, and mental illness. https://en.wikipedia.org/wiki/Obesity | disease of metabolism/acquired metabolic disease/ nutrition disease/overnutrition | Details |
Drug ID | Drug Name | Type | DrugBank ID | Targets | Category | Latest Progress | |
---|---|---|---|---|---|---|---|
D155 | Glucagon | Biological drug | DB00040 | GCGR agonist | Antidiabetic drug | Under clinical trials | Details |
D182 | Insulin | Biological drug | DB00030 | INSR agonist; CPE modulator&product of | -- | Under clinical trials | Details |
D094 | Cysteamine | Chemical drug | DB00847 | GSS stimulant | Renal drug | Under clinical trials | Details |
D095 | Cysteamine bitartrate | Chemical drug | DB00847 | -- | -- | Under clinical trials | Details |