Although ginseng has been shown to have an antiobesity effect, antiobesity-related mechanisms are complex and have not been completely elucidated. In the present study, we evaluated ginseng’s effects on food intake, the digestion, and absorption systems, as well as liver, adipose tissue, and skeletal muscle in order to identify the mechanisms involved. A review of previous in vitro and in vivo studies revealed that ginseng and ginsenosides can increase energy expenditure by stimulating the adenosine monophosphate-activated kinase pathway and can reduce energy intake. Moreover, in high fat diet-induced obese and diabetic individuals, ginseng has shown a two-way adjustment effect on adipogenesis. Nevertheless, most of the previous studies into antiobesity effects of ginseng have been animal based, and there is a paucity of evidence supporting the suggestion that ginseng can exert an antiobesity effect in humans.

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Microbiota contribute to the induction of type 2 diabetes by high-fat/high-sugar (HFHS) diet, but which organs/pathways are impacted by microbiota remain unknown. Using multiorgan network and transkingdom analyses, we found that microbiota-dependent impairment of OXPHOS/mitochondria in white adipose tissue (WAT) plays a primary role in regulating systemic glucose metabolism. The follow-up analysis established that Mmp12+ macrophages link microbiota-dependent inflammation and OXPHOS damage in WAT. Moreover, the molecular signature of Mmp12+ macrophages in WAT was associated with insulin resistance in obese patients. Next, we tested the functional effects of MMP12 and found that Mmp12 genetic deficiency or MMP12 inhibition improved glucose metabolism in conventional, but not in germ-free mice. MMP12 treatment induced insulin resistance in adipocytes. TLR2-ligands present in Oscillibacter valericigenes bacteria, which are expanded by HFHS, induce Mmp12 in WAT macrophages in a MYD88-ATF3–dependent manner. Thus, HFHS induces Mmp12+ macrophages and MMP12, representing a microbiota-dependent bridge between inflammation and mitochondrial damage in WAT and causing insulin resistance.

BackgroundPrevious studies have shown that both ginseng root and ginseng berry exhibit antiobesity and antidiabetic effects. However, a direct comparison of the efficacy and mechanisms between the root and the berry after oral administration remains to be illuminated.MethodsIn this study, we observed the effects of fermented ginseng root (FGR) and fermented ginseng berry (FGB) on obesity and lipid metabolism in high-fat diet induced obese mice.ResultsFGR and FGB significantly inhibited the activity of pancreatic lipase in vitro. Both FGR and FGB significantly suppressed weight gain and excess food intake and improved hypercholesterolemia and fatty liver, while only FGR significantly attenuated hyperglycemia and insulin resistance. Both FGR and FGB significantly inhibited the mRNA expression of Ldlr and Acsl1 while FGR also significantly inhibited expression of Cebpa and Dgat2 in liver. FGR significantly decreased the epididymal fat weight of mice while FGB significantly inhibited the mRNA expression of genes Cebpa, Fas, Hsl, Il1b, and Il6 in adipose tissue.ConclusionSaponin from both FGR and FGB had a beneficial effect on high-fat diet-induced obesity. Compared to FGB, FGR exhibited more potent antihyperglycemic and antiobesity effect. However, only FGB significantly inhibited mRNA expression of inflammatory markers such as interleukins 1β and 6 in adipose tissue.

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To transform ginsenosides, Korean ginseng berry (KGB) was fermented by mycotoxin non-producing Aspergillus niger and Aspergillus oryzae. Changes of ginsenoside profile and anti-proliferative activities were observed. Results showed that A. niger tended to efficiently transform protopanaxadiol (PPD) type ginsenosides such as Rb1, Rb2, Rd to compound K while A. oryzae tended to efficiently transform protopanaxatriol (PPT) type ginsenoside Re to Rh1 via Rg1. Butanol extracts of fermented KGB showed high cytotoxicity on human adenocarcinoma HT-29 cell line and hepatocellular carcinoma HepG2 cell line while that of unfermented KGB showed little. The minimum effective concentration of niger-fermented KGB was less than 2.5 µg/mL while that of oryzae-fermented KGB was about 5 µg/mL. As A. niger is more inclined to transform PPD type ginsenosides, niger-fermented KGB showed stronger anti-proliferative activity than oryzaefermented KGB.

Bifidobacterium animalis subsp. lactis AD011 catalyzed >85% of quercetin-3-glucoside and isorhamnetin-3-glucoside into quercetin (Q) and isorhamnetin (IR), respectively, in 2 h. These Q and IR showed improved anti-inflammatory activity.

Ginseng and probiotics have anti-obesity effects in mice fed a high-fat diet (HFD). Absorption of ginsenoside and colonization of probiotics occur in the intestine. In this study, a mixture of fermented ginseng and two probiotics, BORI and CH88, was administered to HFD-fed mice for 9 weeks. The mixture significantly suppressed weight gain ( < 0.05, = 8) and lipid deposition in the liver and adipose tissues as well as increased the mice's food intake. The adipocyte size of the adipose tissue was significantly decreased in the mixture-fed group, especially when 0.5% fermented ginseng and 5 × 10⁸/ml of the two probiotics were used ( < 0.05, = 10). The expression of TNF-α in adipose tissue was efficiently downregulated in the mixture-fed group ( < 0.05, = 4). The supplement also improved the mice's fasting blood glucose levels ( < 0.05, = 8) and total cholesterol feces excretion ( < 0.05, = 8). The mixture of fermented ginseng and BORI and CH88 could have an anti-obesity effect and suppress lipid deposit in the liver and adipose tissues.