Retracted: Effects of (−)‐hydroxycitric acid on lipid droplet accumulation in chicken embryos

Abstract

This study was conducted to determine the impact of (-)-hydroxycitric acid ((-)-HCA) on biochemical indices and lipid metabolism parameters in chicken embryos. Two hundred and forty fertilized eggs were divided into six groups and injected with (-)-HCA at concentrations of 0, 0.1, 0.5, 1.0, 10.0 and 50 mg/kg (n = 40). After 19 days of incubation, serum and liver were collected for analysis of biochemical indices and lipid metabolism parameters. Results showed no significant differences on serum biochemical indices: 1-50 mg/kg (-)-HCA significantly increased serum glucose and hepatic glycogen contents (P < 0.05). Oil Red O staining analysis showed total area, counts of lipid droplets and hepatic triglyceride content were significantly decreased (P < 0.01), meanwhile hepatic lipase and lipoprotein lipase activity were significantly increased (P < 0.05). ACLY, ME1, SREBP-1c messenger RNA (mRNA) levels in 0.5-10 mg/kg groups and FAS mRNA level in 1-10 mg/kg groups were significantly decreased (P < 0.05), while PPARα mRNA level, serum adiponectin content and AdipoR1 mRNA level were significantly increased in 0.5-50 mg/kg groups (P < 0.05). These results indicated (-)-HCA treatment inhibited triglyceride synthesis via decreasing lipogenesis-related factors, mRNA expression level and accelerated lipolysis by enhancing lipoprotein lipase and hepatic lipase activity, which finally reduced lipid droplet accumulation, and this action may be associated with activating the adiponectin signaling pathway.

Selected Physiological Effects of a Garcinia Gummi-Gutta Extract in Rats Fed with Different Hypercaloric Diets

“…Unfortunately, reports on the hypoglycemic mechanisms exerted by GGG on HCA are scarce. Brandt et al [ 17 ] found that HCA did not ameliorate hypertriglyceridemia, plasma insulin or liver glycogen levels when co-administered with a HS diet (50% fructose w/w ); however, in chicken embryos, HCA significantly increased plasma glucose but also hepatic glycogen [ 46 ], implicating some sort of efficient anabolic utilization of glucose that should be further investigated. Also, compared to non-supplemented diets, urinary ketones were substantially reduced with GGG rind extract-supplemented diets, although the fecal fat excretion did not change.…”

“…The best anti-adiposity effect (evaluated by DXA) was seen in the HF+ group (12–20%) and the severity of hepatocyte lipidosis was HF > control > HF+. Oral administration of HCA significantly reduces in vivo lipogenic rates in a dose-dependent-manner in the liver, adipose tissue and small intestine of rats, a process involving ATP-citrate lyase inhibition [ 43 ], while in chicken embryos, HCA inhibits TAG hepatic synthesis by well-orchestrated events that include accelerated lipolysis by enhancing lipoprotein-lipase, hepatic-lipase, and transactivation of the adiponectin signaling pathway [ 46 ]. Also, in broiler chickens, HCA reduces abdominal fat deposition by regulation at the transcriptional level, not only ATP-citrate lyase but also fatty acid synthase, PPARα, and SREBP-1c [ 47 ]; even when those mechanisms are plausible, the epigenetic effects in normal and obese rats deserve further investigation.…”

Age-Related Changes in Serum Lipid Levels, Hepatic Morphology, Antioxidant Status, Lipid Metabolism Related Gene Expression and Enzyme Activities of Domestic Pigeon Squabs (Columba livia)

“…Besides being synthesized in the liver, almost all the lipids which accumulate in the body are derived from the diet [7]. Since lipid intake changes with age, as an atherosclerosis-susceptible breed [8][9][10], Columba squabs might have age-related alteration in lipid metabolism.…”

Potential role of ALDH3A2 on the lipid and glucose metabolism regulated by (‐)‐hydroxycitric acid in chicken embryos

“…Thus, we conjectured that ALDH3A2 might participated in the energy metabolism regulated by (‐)‐HCA in chicken embryos. Our previous study showed that (‐)‐HCA increased hepatic glycogen content and promoted gluconeogenesis in chicken (Peng, Li, Yu, Ge, & Ma, ). Lim, Ryu, Suh, Ishihara, and Fushiki () found that (‐)‐HCA promoted gluconeogenesis and modestly increased liver glycogen in rats.…”

“…PFK-1, one of the rate-limiting enzyme in glycolysis, catalyzes the fructose-6-phosphate convert into fructose 1,6-bisphosphate (Shen et al, 2016). Our previous study showed that (-)-HCA increased hepatic glycogen content and promoted gluconeogenesis in chicken (Peng, Li, Yu, Ge, & Ma, 2018). **p < 0.01 and *p < 0.05, relative to shNC group; # p < 0.05 and ## p < 0.01, relative to (-)-HCA alone treatment group; NS, indicated no difference As known, SDH is the only membrane enzyme that participates in both citric acid cycle and electron transport chain (Rutter, Winge, & Schiffman, 2010).…”