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According to Chinese medicine theory, Yang/Qi plays
a pivotal role in driving physiological functions in the body, these being
highly dependent on mitochondrial ATP production. Consistent with this,
Yang/Qi-invigorating Chinese tonifying herbs have been found to stimulate
mitochondrial ATP generation capacity (ATP-GC) in H9c2 cardiomyocytes. In the
present study, we have demonstrated that Yang-invigorating Chinese tonifying
herbs (namely, Eucommiae Cortex, Cibotii Rhizoma, Dipsaci Radix, Cynomorii Herba,
Cistanches Herba, Cuscutae Semen, EpimediiHerba and Morindae Radix) and
Qi-invigorating Chinese tonifying herbs (namely, Ginseng Radix,
Pseudostellariae Radix, Quinquefolii Radix, Codonopsis Radix, Astragali Radix,
Atractylodis Rhizoma, Juiubae Fructus, Fici Simplicissimae Radix and Dioscoreae
Oppositae Radix) act by different mechanisms to stimulate mitochondrial ATP-GC.
While Yang-invigorating herbs fluidize mitochondrial membranes and thus stimulate ATP-GC, Qi-invigorating herbs
can enhance cellular glutathione status and increase ATP-GC. The different
mechanisms by which Yang-invigorating herbs and Qi-invigorating herbs stimulate
mitochondrial ATP-GC may serve as the basis for establishing biomarkers
for Yang/Qi-invigorating herbs and herbal health products in general.
Obesity is a risk factor for metabolic disorders, with its prevalence being increased in the world over the past several decades. Therapeutical interventions for obesity are thus urgently needed. In the present study, we investigated the effect of long-term treatment (0.51 and 5.1 g/kg/day, 5 days per week for a total of 40 doses) with an herbal formula MCC [which comprises the fruit of Momordica charantia (MC), the pericarpium of Citri reticulata and L-carnitine] in normal diet (ND) and high fat diet (HFD)-fed female ICR mice. Body weight change was monitored during the course of the experiment. Fat pad indices, plasma glucose and lipid contents, as well as metabolic enzyme activities and mitochondrial coupling efficiency in skeletal muscle were measured at 24 hours after the last dosing. Results showed that HFD increased the body weight, fat pad indices, plasma glucose and lipid contents as well as β-hydroxyacyl-Co A dehydrogenase (β-HAD) and carnitine palmitoyl CoA transferase (CPT) activities in skeletal muscle. However, the phosphofructokinase (PFK) activity was decreased in skeletal muscle. MCC treatment reduced the HFD-induced increases in body weight, fat pad indices and plasma lipid contents. MCC treatment only partially reversed the HFD-induced changes in β-HAD and CPT activities, but did not restore the HFD-induced decrease in PFK activity. MCC did not alter the plasma glucose level and mitochondrial coupling efficiency in skeletal muscle of ND and HFD-fed mice. Since MCC formula did not increase activities of energy metabolic enzymes or induce mitochondrial uncoupling, the weight loss effect of MCC is likely related to the reduction of intestinal lipid absorption in HFD-fed
Obesity has been found to be associated with increased incidence of various metabolic disorders. Anti-obesity interventions are therefore urgently needed. An earlier study has demonstrated that treatment with an herbal formula MCC, which comprises the fruit of Momordica charantia (MC), the pericarpium of Citri reticulate (CR) and L-carnitine (CA), reduced the weight gain in high fat diet (HFD)-fed mice. In the present study, we investigated the effect of long-term treatment with MCC (6 g/kg/day × 40 doses) and various combinations of its constituents in HFD-fed female ICR mice. Body weight change was monitored during the course of the experiment. Total and differential adiposity, plasma lipid contents, metabolic enzyme activities and mitochondrial coupling efficiency in skeletal muscle were measured. Glucose homeostasis was also assessed. Results showed that HFD increased the body weight, total and differential adiposity, and plasma lipid contents as well as impaired metabolic status in skeletal muscle and glucose homeostasis. MCC and all combinations of its constituents reduced the weight gain in HFD-fed mice, which was accompanied with an improvement on glucose homeostasis. While MC, CA and CR independently suppressed the HFD-induced weight gain in mice, MC seems to be the most effective in weight reduction, all of which correlated with the induction of mitochondrial uncoupling in skeletal muscle. Only CA and CR, but not MC, significantly reduced the total adiposity and visceral adiposity as well as plasma cholesterol level. However, the two component combinations, MC + CR and MC + CA, decreased the degree of visceral adiposity and plasma cholesterol level, respectively. MCC treatment at 1.5 g/kg (but not a higher dose of 6 g/kg) suppressed visceral adiposity and induced mitochondrial uncoupling in skeletal muscle in HFD-fed mice. The finding suggests that MCC may offer a promising prospect for ameliorating the diet-induced obesity and metabolic disorders in humans.