Inflammation has been implicated in the hypothalamic leptin and insulin resistance resulting defective food intake during high fat diet period. To investigate hypothalamic inflammation in dietary induced obesity (DIO) and obesity resistant (DIO-R) rats, we established rat models of DIO and DIO-R by feeding high fat diet for 10 weeks. Then we switched half of DIO and DIO-R rats to chow food and the other half to high fat diet for the following 8 weeks to explore hypothalamic inflammation response to the low fat diet intervention. Body weight, caloric intake, HOMA-IR, as well as the mRNA expression of hypothalamic TLR4, NF-κB, TNF-α, IL-1β, and IL-6 in DIO/HF rats were significantly increased compared to DIO-R/HF and CF rats, whereas IL-10 mRNA expression was lower in both DIO/HF and DIO-R/HF rats compared with CF rats. Switching to chow food from high fat diet reduced the body weight and improved insulin sensitivity but not affecting the expressions of studied inflammatory genes in DIO rats. Take together, upregulated hypothalamic inflammation may contribute to the overeating and development of obesity susceptibility induced by high fat diet. Switching to chow food had limited role in correcting hypothalamic inflammation in DIO rats during the intervention period.

Reducing diet fat or replacing lard oil with soybean oil in high-fat diet alleviates obesity-related inflammation and insulin resistance by attenuating the upregulation of OPN and macrophage infiltration into adipose tissue induced by high-fat diet.

ScopesTo investigate the effects of high-fat diet enriched with lard oil or soybean oil on liver endoplasmic reticulum (ER) stress and inflammation markers in diet-induced obese (DIO) rats and estimate the influence of following low-fat diet feeding.Methods and ResultsMale SD rats were fed with standard low-fat diet (LF, n = 10) and two isoenergentic high-fat diets enriched with lard (HL, n = 45) or soybean oil (HS, n = 45) respectively for 10 weeks. Then DIO rats from HL and HS were fed either high-fat diet continuously (HL/HL, HS/HS) or switched to low-fat diet (HL/LF, HS/LF) for another 8 weeks. Rats in control group were maintained with low-fat diet. Body fat, serum insulin level, HOMA-IR and ectopic lipid deposition in liver were increased in HL/HL and HS/HS compared to control, but increased to a greater extent in HL/HL compared to HS/HS. Markers of ER stress including PERK and CHOP protein expression and phosphorylation of eIF2α were significantly elevated in HL/HL group while phosphorylation of IRE1α and GRP78 protein expression were suppressed in both HL/HL and HS/HS. Besides, inflammatory signals (OPN, TLR2, TLR4 and TNF-α) expressions significantly increased in HL/HL compared to others. Switching to low-fat diet reduced liver fat deposition, HOMA-IR, mRNA expression of TLR4, TNF-α, PERK in both HL/LF and HS/LF, but only decreased protein expression of OPN, PERK and CHOP in HL/LF group. In addition, HL/LF and HS/LF exhibited decreased phosphorylation of eIF2α and increased phosphorylation of IRE1α and GRP78 protein expression when compared with HL/HL and HS/HS respectively.ConclusionsLard oil was more deleterious in insulin resistance and hepatic steatosis via promoting ER stress and inflammation responses in DIO rats, which may be attributed to the enrichment of saturated fatty acid. Low-fat diet was confirmed to be useful in recovering from impaired insulin sensitivity and liver fat deposition in this study.

Seed germination is a critical stage and the first step in the plant’s life cycle. H2O2 and Ca2+ act as important signal molecules in regulating plant growth and development and in providing defense against numerous stresses; however, their crosstalk in modulating seed germination remains largely unaddressed. In the current study, we report that H2O2 and Ca2+ counteracted abscisic acid (ABA) to induce seed germination in melon and Arabidopsis by modulating ABA and gibberellic acid (GA3) balance. H2O2 treatment induced a Ca2+ influx in melon seeds accompanied by the upregulation of cyclic nucleotide-gated ion channel (CNGC) 20, which encodes a plasma membrane Ca2+-permeable channel. However, the inhibition of cytoplasmic free Ca2+ elevation in the melon seeds and Arabidopsis mutant atcngc20 compromised H2O2-induced germination under ABA stress. CaCl2 induced H2O2 accumulation accompanied by the upregulation of respiratory burst oxidase homologue (RBOH) D and RBOHF in melon seeds with ABA pretreatment. However, inhibition of H2O2 accumulation in the melon seeds and Arabidopsis mutant atrbohd and atrbohf abolished CaCl2-induced germination under ABA stress. The current study reveals a novel mechanism in which H2O2 and Ca2+ signaling crosstalk offsets ABA to induce seed germination. H2O2 induces Ca2+ influx, which in turn increases H2O2 accumulation, thus forming a reciprocal positive-regulatory loop to maintain a balance between ABA and GA3 and promote seed germination under ABA stress.