Key result
ApoA-IV deficiency increases adiposity by ~14 percentage points in high-fat-diet-fed female mice.
Why the study?
The study was conducted to determine the impact of apoA-IV deficiency on metabolic functions in female 129X1/SvJ mice.
Does apoA-IV deficiency increase susceptibility to diet-induced obesity and alter metabolic function in female 129X1/SvJ mice?
Does apoA-IV deficiency increase susceptibility to diet-induced obesity and alter metabolic function in female 129X1/SvJ mice?
Female apoA-IV deficient mice on a 129X1/SvJ background serve as a novel preclinical model demonstrating increased susceptibility to diet-induced obesity and insulin resistance due to decreased energy expenditure.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications; leaves open apoA-IV's role in human metabolic disease.
Obesity is one of the main risk factors for cardiovascular diseases, type II diabetes, hypertension, and certain cancers. Obesity in women at the reproductive stage adversely affects contraception, fertility, maternal well-being, and the health of their offspring. Being a major protein component in chylomicrons and high-density lipoproteins, apolipoprotein A-IV (apoA-IV) is involved in lipid metabolism, food intake, glucose homeostasis, prevention against atherosclerosis, and platelet aggregation. The goal of the present study is to determine the impact of apoA-IV deficiency on metabolic functions in 129X1/SvJ female mouse strain. After chronic high-fat diet feeding, apoA-IV−/− mice gained more weight with a higher fat percentage than wild-type (WT) mice, as determined by measuring their body composition. Increased adiposity and adipose cell size were also observed with a microscope, particularly in periovarian fat pads. Based on plasma lipid and adipokine assays, we found that obesity in apoA-IV−/− mice was not associated with hyperlipidemia but with higher leptin levels. Compared to WT mice, apoA-IV deficiency displayed glucose intolerance and elevated insulin levels, according to the data of the glucose tolerance test, and increased HOMA-IR values at fasting, suggesting possible insulin resistance. Lastly, we found obesity in apoA-IV−/− mice resulting from reduced energy expenditure but not food intake. Together, we established a novel and excellent female mouse model for future mechanistic study of obesity and its associated comorbidities.
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Qu et al. (2023) studied Diet-induced obesity and insulin resistance (preclinical model). Apolipoprotein A-IV deficiency (apoA-IV-/-) vs. Wild-type (WT) mice was evaluated on Fat percentage after 16 weeks of high-fat diet feeding. Apolipoprotein A-IV deficiency in female mice fed a high-fat diet significantly increased adiposity, body weight, and insulin resistance compared to wild-type mice.
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