Adipogenesis is a complex physiological process involving the formation of adipocytes and accumulation as adipose tissues.
It is one of the contributors for the development of obesity. This study assessed the potential of phenolic extracts and potassium hydroxycitrate, obtained from Hibiscus sabdariffa, to inhibit adipogenesis.
The phenolic extracts were obtained using organic solvents (methanol, ethanol and ethyl acetate) and water individually.
Results showed that phenolic extracts were able to reduce lipid accumulation by about 95% in hADSCs, while potassium hydroxycitrate did not show any reduction. All the phenolic extracts downregulated the gene expression of two key adipogenic markers (PPAR-γ and aP2). Ethanol extracts exhibited the highest downregulation of PPAR-γ and aP2 by 3 and 10 times, respectively.
There was no improvement in the anti-adipogenic potential when the phenolic extract was combined with potassium hydroxycitrate confirming that phenolic compounds were responsible for the inhibition of adipogenesis.
These results indicate that phenolic extracts from H. sabdariffa have potential to regulate the expression of adipogenic genes and restrict the lipid accumulation in mature adipocytes. Thus, phenolic extracts can be used in formulations intended to manage obesity.
reference link : https://ifst.onlinelibrary.wiley.com/doi/10.1111/ijfs.16269
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In the present study, we demonstrated the anti-obesity and liver-protection potential of H. sabdariﬀa extract (HSE).
HSE decreased body weight, BMI and body fat, and reduced abdominal fat distribution. HSE decreased serum FFA, exerting a beneficial eﬀect on metabolic regulation, while improving the liver steatosis.
Noticeably, the safety evaluation revealed that HSE did not harm the human body. This is the first study to investigate HSE for the attenua- tion of human obesity and fatty liver.
BMI is one of the most popular anthropometric indices. In 2000, WHO defined the BMI cut-oﬀ points as 23 kg m 2 (over- weight), 25 kg m 2 (obesity class I), and 30 kg m 2 (obesity class II) for people living in the Asia Pacific region. All the subjects in the trial had a BMI > 25 kg m 2 (obesity class I) and had been diagnosed with fatty liver for more than one year.
However, although the BMI is widely used and adopted in this study, it may still have limitations. For some populations who have shorter lower limbs, using standing height alone may over- estimate the number of individuals that are overweight and obese, and at risk for type 2 diabetes mellitus and cardiovascular disease.18
On the contrary, central obesity predicts a high prevalence of hepatic steatosis and related disorders. A previous analysis revealed that the waist circumference and waist/height ratio had a significant association with the development of fatty liver, whereas the BMI did not. In this study, we measured the waist circumference and used the waist-to-hip ratio as an index, which should more adequately reflect the regulatory eﬀect of HSE on abdominal fat distribution and central obesity.19
Non-alcoholic fatty liver is generally considered to be the liver component of metabolic syndrome, including an excessive waist circumference, dyslipidaemia, hyperglycaemia, and hypertension.20 In a clinical situation, the ultrasonic examination of fatty liver is usually qualitative but not quantitative.
To overcome this limitation, we cited and mimicked the semi-quantitative FS scores, and demonstrated the eﬀect of HSE on improving fatty liver.21
H. sabdariﬀa improved the lipid profiles of patients with metabolic syndrome.22
Recently, HSE was reported to prevent hepatic steatosis through down-regulation of PPAR-g and SREBP-1c, which plays an important role in obesity-induced inflammation, especially in the liver, adipose tissue, and vascular system.23,24
According to the previous report, the calyx of H. sabdariﬀa L. is rich in polyphenols, including anthocyanins, flavonoids and phenolic acids.25 H. sabdariﬀa polyphenols prevented hyperglycemia and hyperlipidemia, inhibited hepatic lipogenesis, while they promoted hepatic lipid clearance.26,27
Many of them, such as gallic acid derivative, chlorogenic acid, caﬀeic acid, quercetin, and tiliroside, were demonstrated to be eﬀective on reducing obesity and related disorders (Table 4). Galloyl ester decreased the body weight, liver weight, and hepatic lipid.28 Chlorogenic acid lowered serum cholesterol and attenuated fatty liver by up-regulating the expression of PPAR-a.29
Chlorogenic acid and caﬀeic acid improved body weight, lipid metabolism and obesity-related hormone levels in high-fat fed mice.30 Recently, it was reported that caﬀeic acid inhibits hepatic lipogenesis but promotes lipolysis via regulating AMPK in HepG2 cells.31
Non-alcoholic fatty liver disease rats (NAFLD) have higher serum levels of IL-18 but lower levels of IL-10 than their healthy counterparts. Quercetin treatment reversed the cytokine expressions and helped to delay the progression of NAFLD.32
An in vitro experiment showed that quercetin exerts anti-adipogenesis activity by activating the AMPK signal pathway in 3T3-L1 preadipocytes, while it induces the apoptosis of mature adipocytes by modulation of the ERK and JNK path- ways.33 Tiliroside, a glycosidic flavonoid, ameliorates hyper- insulinemia and hyperlipidemia in obese-diabetic mice by activating adiponectin signaling and the hepatic lipid oxidation.34
In addition, anthocyanins contained in H. sabdariﬀa L. could exert anti-obesity and liver-protective eﬀects. It was reported that purified anthocyanins reduced the body weight and body fat of rats fed with a high-fat diet.35
Recently, Wu et al. reported that anthocyanins inhibit body weight gain, reduce insulin resistance, increase serum adiponectin while decrease leptin, lower the adipocytes and lipid accumulation, improve serum and liver lipid profiles, and ameliorate the impaired hepatic function in diet-induced obese mice.36,37
Under normal circumstances, anthocyanins even have the capability to reduce body weight and food intake through its modulation of NPY and GABAB1R in the hypothalamus.38
Some literature has reported that branched chain-amino acids are associated with obesity and insulin resistance.39
We have analyzed the amino acid composition of HSE (Table 5), whereas only aspartic is obviously high. Hence the clinical eﬀect of HSE should mainly be attrib- uted to the polyphenols.
In this trial, aer HSE treatment, no significant diﬀerence was observed in the lipid profile except for FFA. These results are in accordance with that of Kuriyan, Kumar and Kurpad (2010),40 which might attribute to the dose of HSE (1 g day 1) being too low.
The optimum dose of HSE intake should be determined in future clinical work. Further research on the bioavailability and pharmacokinetics of HSE is needed. In conclusion, HSE has the potential to act as an adjuvant for preventing obesity and related fatty liver.