BackgroundThe incidence of the insulin resistance syndrome has increased at an alarming rate worldwide, creating a serious challenge to public health care in the 21st century. Recently, epidemiological studies have associated the prevalence of type 2 diabetes with elevated body burdens of persistent organic pollutants (POPs). However, experimental evidence demonstrating a causal link between POPs and the development of insulin resistance is lacking.ObjectiveWe investigated whether exposure to POPs contributes to insulin resistance and metabolic disorders.MethodsSprague-Dawley rats were exposed for 28 days to lipophilic POPs through the consumption of a high-fat diet containing either refined or crude fish oil obtained from farmed Atlantic salmon. In addition, differentiated adipocytes were exposed to several POP mixtures that mimicked the relative abundance of organic pollutants present in crude salmon oil. We measured body weight, whole-body insulin sensitivity, POP accumulation, lipid and glucose homeostasis, and gene expression and we performed microarray analysis.ResultsAdult male rats exposed to crude, but not refined, salmon oil developed insulin resistance, abdominal obesity, and hepatosteatosis. The contribution of POPs to insulin resistance was confirmed in cultured adipocytes where POPs, especially organochlorine pesticides, led to robust inhibition of insulin action. Moreover, POPs induced down-regulation of insulin-induced gene-1 (Insig-1) and Lpin1, two master regulators of lipid homeostasis.ConclusionOur findings provide evidence that exposure to POPs commonly present in food chains leads to insulin resistance and associated metabolic disorders.

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A study was undertaken to determine the effect of dietary lipid level on growth, feed efficiency and body chemical composition of juvenile grass carp. Seven isonitrogenous diets (400 g kg−1 crude protein) containing seven dietary lipid level (0, 20, 40, 60, 80, 100 and 120 g kg−1 dry matter) were fed to triplicate groups of 40 fish with initial weight 6.52 g, for 70 days. No obvious and assured essential fatty acid deficiency symptom appeared in fish fed the lipid‐free diet. Excess dietary lipid level (100 and 120 g kg−1) resulted in decreased feed intake. The best growth performance and feed utilization was observed in fish fed 20–40 g kg−1 dietary lipid. The fish fed a lipid‐free diet had the lowest protein efficiency and protein retention. Growth performance and feed utilization increased with the increasing dietary lipid levels up to 40 g kg−1 dietary lipid. Higher dietary level (above 40 g kg−1) made growth performance and feed utilization decrease and no protein sparing effect was observed. Lipid retention decreased as dietary lipid level increased. Mesenteric fat index (MFI) increased, hepatosomatic index (HSI) decreased with dietary lipid level. The increased MFI and simultaneous decrease lipid retention can be explained by differences in growth. The effect of dietary lipid levels on the chemical composition of tissues was significant only for whole body and muscle. The excess lipid content of liver in all groups was regarded as a slight symptom of fatty liver, which was partly identified by microscopic structural study and lower plasma lipid indexes, comparing to the initial plasma data. In conclusion, grass carp is a fish with low energy requirement and excess dietary lipid level should be avoided.

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Herbivorous grass carp (Ctenopharyngodon idella) has been reported to exhibit low capacity to utilize high dietary lipid, but different lipid sources might affect this limited capacity. In order to compare the effects of different lipid sources with different lipid levels, juvenile grass carp were fed one of nine diets containing three oils [lard, plant oil mixed by maize and linseed oil, and n‐3 high unsaturated fatty acid‐enriched (HUFA‐enriched) fish oil] at three lipid levels (20, 60 and 100 g kg−1 dry diet) for 8 weeks. Decreased feed intake, poor growth performance, hepatic pathology and higher blood lipid peroxidation were found in 60 and 100 g kg−1 fish oil groups. Conversely, in lard and plant oil groups, even at 100 g kg−1 dietary lipid level, feed intake and growth performance did not decrease, despite histological observation revealed hepatic pathology in these groups. Plasma triglyceride and cholesterol contents increased significantly in all 100 g kg−1 dietary lipid groups. In the comparison of hepatic FA β‐oxidation among three oil groups at 60 g kg−1 dietary lipid level, impaired mitochondrial and peroxisomal FA oxidation capacity was observed in fish oil group. The results confirmed the relatively low capacity of grass carp to utilize high dietary lipid, and furthermore excess HUFA intake will result in more serious adverse effects than other FA.

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