Evidence-Based Complementary and Alternative Medicine

Evidence-Based Complementary and Alternative Medicine / 2015 / Article
Special Issue

Natural Products for the Treatment of Obesity, Metabolic Syndrome, and Type 2 Diabetes 2014

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Review Article | Open Access

Volume 2015 |Article ID 747982 | 14 pages | https://doi.org/10.1155/2015/747982

Ancient Records and Modern Research on the Mechanisms of Chinese Herbal Medicines in the Treatment of Diabetes Mellitus

Academic Editor: Srinivas Nammi
Received15 Mar 2014
Accepted25 Jun 2014
Published01 Mar 2015

Abstract

Over the past decades, Chinese herbal medicines (CHM) have been extensively and intensively studied through from both clinical and experimental perspectives and CHM have been proved to be effective in the treatment of diabetes mellitus (DM). This study, by searching ancient records and modern research papers, reviewed CHM in terms of their clinical application and principal mechanism in the treatment of DM. We summarized the use of CHM mentioned in 54 famous ancient materia medica monographs and searched papers on the hypoglycemic effect of several representative CHM. Main mechanisms and limitations of CHM and further research direction for DM were discussed. On the basis of the study, we were led to conclude that TCM, as a main form of complementary and alternative medicine (CAM), was well recorded in ancient literatures and has less adverse effects as shown by modern studies. The mechanisms of CHM treatment of DM are complex, multilink, and multitarget, so we should find main hypoglycemic mechanism through doing research on CHM monomer active constituents. Many CHM monomer constituents possess noteworthy hypoglycemic effects. Therefore, developing a novel natural product for DM and its complications is of much significance. It is strongly significant to pay close attention to CHM for treatment of DM and its complications.

1. Introduction

Diabetes mellitus (DM), including type 1 and type 2, has become epidemic worldwide [13], and its incidence has been on rise year by year [4]. Previous reports have demonstrated that overweight, especially obesity at younger ages, substantially increases the risk for DM [1, 58]. The finding is consistent with the description in the “Medical Classic of the Yellow Emperor,” the earliest monumental work on the traditional Chinese medicine (TCM) dating back to the Warring States Period (about 446 B.C.−221 B.C.). DM increases the risk for micro- and macrovascular complications and premature death and poses tremendous socioeconomic burden [2, 4, 9]. In spite of the introduction of insulin and other hypoglycemic agents, so far, no treatment protocols can achieve a complete cure. Moreover, the side effects of these drugs, which are substantial and inevitable, present another challenge.

Complementary and alternative medicine (CAM) have been extensively used in modern times. TCM, as a main form of CAM, has been proved to be effective for the treatment of DM with relatively less side effects in China and beyond [10, 11]. Some hypoglycemic drugs of plant origin have been approved for clinical use by the regulatory authorities in China, such as Yusanxiao, Yijin, and Kelening, among others [12].

The mechanisms of Chinese herbal medicines (CHM) in the treatment of DM have been extensively and intensively studied from biological, immunological, and phytochemical perspectives and great advances have been made in the past decades. This paper reviewed records or descriptions concerning the use of CHM for treatment of DM in ancient Chinese literatures (before 1920 A.D.) and the modern papers on the mechanisms of CHM treating DM. We also compared the CHM used in ancient and modern times, examined the limitations of CHM for treating DM, and discussed the future research trend.

2. Ancient Records on Treatment of DM with TCM

Our search of literatures of TCM (before 1920 A.D. or earlier) failed to find the term “DM.” We found a plenty of records or descriptions about “Xiao Ke,” which, in terms of epidemiology, symptoms, etiology, pathogenesis, and treatment, mimicked those of DM. And it is generally accepted that “Xiao Ke” mentioned in ancient Chinese literature is similar to DM of modern medicine [13]. On basis of this assumption, in this paper, we used DM interchangeably with “Xiao Ke” for the convenience of discussion though they are not strictly equivalents in a number of ways.

2.1. Terminology, Epidemiology, Symptoms, Etiology, and Pathogenesis of “Xiao Ke
2.1.1. Name

In TCM, “Xiao Ke” refers to a cluster of clinical symptoms, including polydipsia, polyphagia, polyuria, emaciation, glucosuria, and fatigue. As aforementioned, “Xiao Ke” is a general term for a condition that resembles DM in terms of symptoms. DM classically was divided into three types: upper, middle, and lower “Xiao Ke.” The upper type (Shang Xiao) is characterized by excessive thirst, the middle type (Zhong Xiao) by excessive hunger, and the lower type (Xia Xiao) by excessive urination [13]. By searching “Xiao Ke,” we retrieved a large number of records concerning “Xiao Ke” in ancient TCM literatures.

2.1.2. Epidemiology

The earliest mention of “Xiao Ke” was in the “Medical Classic of the Yellow Emperor.” The book described that the “Xiao Ke” was mostly found in wealthy, obese individuals who liked food rich in oil or fat and in influential officials who were on pills or “Dan,” as it was termed in the book, a mineral-based synthetic drug, which ancient people believe to be able to make them achieve longevity.

2.1.3. Symptoms

The symptoms can be categorized into two groups: general symptoms and complications. The general symptoms include polydipsia, polyphagia, polyuria, glucosuria, emaciation, dry mouth, hunger, emptiness of the stomach, and frequent urination. And complications include diabetic foot, diabetic retinopathy, lung tuberculosis, diabetic impotence, and diabetic nephropathy. Obviously, those symptoms and complications are extremely similar to DM, as shown in Table 1.


Symptoms of “Xiao Ke” in Zhu Bing Yuan Hou LunaSymptoms of DM in Textbook of Internal Medicine [22]

General
symptoms
Polydipsia; dry mouth and lips; polyphagia; hunger; emptiness of the stomach; frequent urination; polyuria; glucosuria; emaciation; adiposity; fatigue of limbs; mental fatigue; feverish dysphoria; itchy skin; hyperhidrosis; dizziness; sweet feeling in the mouth.Polydipsia; thirst; polyphagia; hunger; polyuria; marasmus; obesity; sweet taste of urine; itchy skin; vulva pruritus; fatigue; lightheadedness.

ComplicationsCarbuncle and soreness; night blindness; internal oculopathy; lung tuberculosis; edema; precordial pain; pectoral stuffiness pain; apoplexy; coma; impotence; foot carbuncle-abscess; unsmooth defecation; diarrhea; anorexia; short breath; waist soreness; dizziness and tinnitus; pachylosis; whitish and turbid urine; muscle atrophy of the lower extremities; oliguria; nightly sweating; coolness of extremities.Carbuncle and furuncle; diabetic retinopathy; pulmonary tuberculosis; diabetic cardiomyopathy; diabetic ketoacidosis; diabetic impotence; glaucoma; diabetic nephropathy; atherosclerosis; cerebral ischemic stroke; diabetic foot; constipation; diarrhea; myophagism; paralysis; oliguria; hyperhidrosis; hypohidrosis or anhidrosis; diabetic gastroparesis.

aThe “Zhu Bing Yuan Hou Lun”: a book describing causes and manifestations of diseases by Yuanfang Chao, a famous TCM doctor born about AD 550 and died in 630 A.D. in the Sui Dynasty.
2.1.4. Etiology and Pathogenesis

According to the theory of TCM, the symptoms are essentially caused by “Yin Xu” (Yin deficiency) and “Zao Re” (dryness heat). In TCM there is a belief that Yin deficiency is the “Ben” (origin or root cause) and dryness heat is the “Biao” (symptoms or external manifestations). The Ben or root causes involve the invasion of exogenous pathogens, innate deficiency, intemperance in eating, abnormal emotional states (anger, anxiety, depression, distress, panic, and fear), excessive physical strains (mental or physical exertion and sexual intercourse), or propensity for abusing Dan medicines [11]. Yin and Yang are two opposing aspects of things. For instance, cold, moist, night, structure, and downward mobility belong to Yin while heat, dryness, day, function, and upward mobility belong to Yang [14].

2.2. Treatment

We searched for the term “Xiao Ke” in more than 1,000 TCM ebooks included in Encyclopedia of TCM (Compact Disk, ISBN: 7-900377-49-2/R·8), published by Hunan Electronic and Audiovisual Publishing House. The database contained, among others, “Bencao Gangmu (Compendium of Materia Medica)”, Puji fang, and so forth.

2.2.1. CHM

We also searched the database for Chinese crude drugs for treating “Xiao Ke.” The database contained only 54 monographs on Chinese materia medica. Most CHM treated “Xiao Ke” by “Qing Re” (clearing heat) (Figure 1), “Yang Yin” (nourishing Yin), and “Yi Qi” (replenishing vital energy) (Figure 2). The Latin names of CHM used in the paper were from the website http://www.theplantlist.org/ or http://www.wikipedia.org/.

2.2.2. Foods

Besides, the monographs also mentioned some foods that help treat “Xiao Ke” in Figure 3.

3. Mechanisms by Which CHM Work on DM and Its Complications

We searched the databases of PubMed, Web of Science, MEDLINE, and CNKI and found that less research attention was paid to Chinese herbal compounds while most studies focused on a single herbal medicine.

The mechanisms of CHM in the treatment of DM have been extensively and intensively studied from biological, immunological, and phytochemical perspectives (Tables 2, 3, and 4).


Latin nameFamilyExtracts or
monomers
In vivo/
in vitro
ModelsEffective doses/doses rangeMechanismsToxic effectReferences

Liriope spicata Lour.LiliaceaeCrude polysaccharide, water extractIn vivo BABL/c mice100, 200 mg/KgIIAINO[23]

Ophiopogon japonicus (Thunb.) Ker Gawl.LiliaceaePolysaccharideIn vivo KKAy mice, C57BL/6J mice75, 300 mg/KgIIAIND[24]
PolysaccharideIn vivo Ob/ob mice300 mg/KgIIAIND[25]

Astragalus membranaceus (Fisch.) BungeLeguminosaePolysaccharideIn vivo KKAy mice, C57BL/6J mice700 mg/KgIIAIND[26]
PolysaccharideIn vivo C57BL/6J mice100, 400 mg/KgPIPRND[27]
PolysaccharideIn vivo Sprague-Dawley (SD) rats 700 mg/KgIHSGND [28]
In vitro C2C12 cells0.05–0.2 mg/mLYES, <200 µg/mL
Astragaloside IVIn vivo SD rats1, 5 mg/KgBLIRND[29]
CalycosinIn vitro Human umbilical vein endothelial cells0.01 µmolBLIRND[30]

Panax ginseng C. A. Mey.AraliaceaeMalonyl ginsenosidesIn vivo Wistar rats50, 100 mg/KgIIAIND[31]
Ginsenoside Rh2In vivo Wistar rats1 mg/KgPIEIND[32]
GinsenosideIn vitro SD rats islet0.1–1 mg/mLPIEI ND[33]
Aqueous extractIn vivo Goto-Kakizaki rats, Wistar rats200 mg/KgPIEI, PIPR, PRGUND[34]
Ginsenoside ReIn vivo SD rats20 mg/KgBLIRND[35]

Panax pseudoginseng Wall.AraliaceaePanax notoginosideIn vivo Wistar rats100, 200 mg/KgCOSRND[36]

Poria cocos (Schw.) Wolf PolyporaceaeCrude extractIn vivo C57BL/KsJ-db/db mice, C57BL/6J mice50 mg/Kg IIAI ND [37]
Dehydrotumulosic acid, dehydrotrametenolic acid, pachymic acid, triterpenes1, 5, 10 mg/Kg

Dioscorea oppositifolia L.DioscoreaceaeDecocted waterIn vivo Wistar rats4 mg/KgIIAIND[38]
PolysaccharoseIn vivo Kun Ming mice4.5 g/KgRAARND[39]

Schisandra chinensis (Turcz.) Baill. Schisandraceae LignanIn vivo SD rats200 mg/Kg IIAI, IHSG, PRGU ND [40]
In vitro 3T3-L1 adipocytes,
Min6 cells, human embryo kidney 293 cells,
0.5, 5 µg/mL

Ophiocordyceps sinensis (Berk.) G. H. Sung, J. M. Sung, Hywel-Jones, and SpataforaClavicipitaceaePolysaccharideIn vivo BALB/c mice, SD rats200, 400 mg/KgPIEI ND[41]
solid-state fermented myceliumIn vivo KK/HIJ mice300 mg/KgPIPRND[42]

Cornus Officinalis Siebold
and Zucc
CornaceaeMethanol extractIn vitro BRIN-BD11 cells, H4IIE cells0–25 µg/mLPIEI, PIPR, IHSGYES, cytotoxicity[43]
Proanthocyanidins In vivo Wistar rats 20 mg/KgINGAND [44]
In vitro α-Glucosidase1.2–2.1 µg/mL

Polygonatum odoratum
(Mill.) Druce
LiliaceaeTotal flavonoidsIn vivo Kun Ming mice, SD rats50, 100, 200 mg/KgPIEIND[45]
Flavonoid, saponinIn vivo SD rats 500 mg/KgCOSR, INGANO[46]

Atractylodes macrocephala Koidz.CompositaeAtractylenolide, amino acidIn vivo Kun Ming mice1.8 g/KgRAARND[39]

Codonopsis pilosula
(Franch.) Nannf.
CampanulaceaeSaccharides, amino acidIn vivo Kun Ming mice4.5 g/KgRAARND[39]

Panax quinquefolius L.AraliaceaeGinsenosideIn vitro Rat pancreatic β cell derived cell line, INS-15, 125, 250 µg/µLPIPR, PIEIND[47]

Rehmannia glutinosa Steud. ScrophulariaceaeCatalpolIn vivo Wistar rats0.1 mg/KgIHSGND[48]
CatalpolIn vitro THP-1 cells100, 300, 500 µmolCOSR, BLIRNO[49]

Dendrobium moniliforme
(L.) Sw.
PunicaceaeWater extractIn vivo NIH mice, SD rats125, 250, 500, 1000 mg/KgINSG, IHSG, PIEIND[50]

Dendrobium chrysotoxum Lindl.PunicaceaePolysaccharideIn vivo BALB/c mice,200, 500 mg/KgCOSRND [51]
In vitro Mouse splenocytes, Jurkat cell, MCF-7 cells0–200 µg/mL

Ganoderma lucidum
(Leyss. ex Fr.) Karst
PolyporaceaePolysaccharidesIn vivo Albino Swiss mice50, 100, 200 mg/KgPIPR, COSRNO [52]
In vitro Wistar rat islets25–100 µg/mL

IIAI: CHM increase insulin sensitivity and ameliorate insulin resistance; PIEI: CHM promote insulin secretion and elevate serum insulin levels; INGA: CHM inhibit α-glucosidase activity; PIPR: CHM protect islet β cells and promote their regeneration; IHSG: CHM increase hepatic glycogen content and suppress gluconeogenesis; INSG: CHM inhibit the secretion of glucagon; PRGU: CHM promote the glucose uptake by adipose and muscular tissues. COSR: CHM control oxidative stress response, such as scavenging oxygen radicals, preventing lipid peroxidation, or inhibiting nitric oxide synthesis; RAAR: CHM regulate the activity of aldose reductase; BLIR: CHM block inflammatory response. NO means not toxic. ND means no data available. YES means toxic.

Latin nameFamily Extracts or monomersIn vivo/
in vitro
ModelsEffective doses/doses rangeMechanismsToxic effectReferences

Paeonia x suffruticosa AndrewsPaeoniaceaePaeonolIn vivo Newborn Wistar rats200, 400 mg/Kg PRGU, INGA ND [53]
In vitro Intestinal brush border membrane vesicles, rat hepatoma cell line H4IIE, human skin fibroblasts cell line Hs68, mouse adipocytes 3T3-L10.01–1 mg/mL,
Polysaccharide-2bIn vivo Wistar rats60 mg/KgIIAIND[54]
Paeonoside, apiopaeonoside, 6-methoxypaeoniflori-genoneIn vitro Human HepG2 cells, HUVECs1–20 µmolIHSGNO[55]

Morus alba L.Moraceae1-Deoxynojirimycin, polysaccharideIn vivo ICR mice150 mg/KgIHSG, PIPRND[56]

Momordica charantia L.CucurbitaceaeSaponin fraction, lipid fractionIn vivo Db/db mice150 mg/KgIIAIND[57]
Protein extractIn vivo Wistar rats 5, 10 mg/KgPIEI, PRGUND [58]
In vitro 3T3-L1 adipocytes, C2C12 cells0.01 µg/mL
Saponins, momordicine II, kuguaglycosideIn vitro MIN6 β cells 0.01–0.125 µg/mLPIEINO[59]
Ethanolic extractIn vivo Albino Wistar rats150, 300 mg/KgPIPR, IHSG, PRGUND[60]
Aqueous extractIn vivo Albino Wistar rats150 mg/KgCOSRND[61]

Pueraria lobata (Willd.) OhwiLeguminosaePuerarinIn vivo SD rats100, 200 mg/KgIIAI ND[62]
DaidzeinIn vivo Kun Ming mice2.3 g/KgINGA, RAARND[39]
PuerarinIn vitro Wistar rats islets100 µmolPIPR, COSRND[63]

Trigonella foenum-graecum L.LeguminosaeHydroalcoholic extractIn vivo C57BL/6J mice2 g/KgIIAI ND[64]
TrigonellineIn vivo Wistar rats40 mg/KgCOSRND[65]
Fenugreek seeds powderIn vivo Albino ratsPowder 5% in rat foodBLIRND[66]

Gardenia jasminoides J. EllisRubiaceaeGeniposideIn vivo C57BL/6J mice200, 400 mg/KgIHSGND[67]

Rheum palmatum L.EmodinIn vivo B6. V- Lepob/Lepob mice25, 50 mg/KgPRGUND [68]
In vitro 3T3-L1 adipocytes3 µmol/L

Acorus calamus L.AraceaeCrude ethanol extractIn vivo Homozygous C57BL/Ks db/db mice100 mg/KgIIAI ND [69]
In vitro L6 rat skeletal muscle cells12.5, 25 µg/mL
Ethyl acetate fractionIn vivo ICR mice400, 800 mg/KgPIEI, INGAND [70]
In vitro HIT-T15 cell line0.41 µg/mL

Eriobotrya japonica (Thunb.) Lindl.RosaceaeCinchonain-IbIn vivo Wister rats108 mg/KgPIEIND [71]
In vitro Rat insulinoma cell line, INS-1 cells0.032 mg/mL

Anemarrhena asphodeloides BungeLiliaceaeTimosaponin, anemaranIn vivo Kun Ming mice1.8 g/KgINGAND[39]
Total saponinsIn vivo SD rats200 mg/KgBLIRND[72]

Lonicera japonica Thunb.CaprifoliaceaeChlorogenic acid, ginnolIn vivo Kun Ming mice2.3 g/KgRAARND[39]

Coptis chinensis Franch.RanunculaceaeBerberine chloride formIn vivo Wistar rats, 125, 500, 250 mg/Kg, INGAND [73]
Beagle dogs80 mg/Kg
In vitro Caco-2 cells 2.5, 10, 40 mg/L
BerberineIn vitro SD rats ventricular myocytes0.1–100 µmol/LCOSRND[74]
BerberineIn vivo Wistar rats100, 200 mg/KgPIPR, COSRND[75]
BerberineIn vivo C57BLKS/J-Leprdb/Leprdb mice, 5 mg/KgIIAIND [76]
Wistar rats380 mg/Kg
In vitro 3T3-L1 cells, L6 cells5 µg/mL

Potentilla discolor BungeRosaceaeFlavonoids, triterpenoidsIn vivo Wistar rats369, 501 mg/KgPIPR, COSRND[77]

Artemisia sphaerocephala Krasch.CompositaeArtemisia sphaerocephala Krasch. gumIn vivo SD rats0.3%, 0.9%, 2.7% gumIIAI, IHSGND[78]

Sophora flavescens AitonLeguminosaeOxymatrineIn vivo Wistar rats60, 120 mg/KgCOSR, BLIRND[79]

Punica granatum L.PunicaceaeMethanolic extractIn vivo Zucker diabetic fatty rats, Zucker lean rats100–500 mg/KgINGAND [80]
In vitro α-glucosidase0.5–32 µg/mL

Arctium lappa L.CompositaeArctigeninIn vivo C57BL/6J mice, B6. V-Lepob/Lepob mice200, 25 mg/KgIHSG, PRGUND [81]
In vitro L6 myotubes0.1–3 µg/mL

IIAI: CHM increase insulin sensitivity and ameliorate insulin resistance; PIEI: CHM promote insulin secretion and elevate serum insulin levels; INGA: CHM inhibit α-glucosidase activity; PIPR: CHM protect islet β cells and promote their regeneration; IHSG: CHM increase hepatic glycogen content and suppress gluconeogenesis; INSG: CHM inhibit the secretion of glucagon; PRGU: CHM promote the glucose uptake by adipose and muscular tissues. COSR: CHM control oxidative stress response, such as scavenging oxygen radicals, preventing lipid peroxidation, or inhibiting nitric oxide synthesis; RAAR: CHM regulate the activity of aldose reductase; BLIR: CHM block inflammatory response. NO means not toxic. ND means no data available. YES means toxic.

Latin nameFamily Extracts or monomersIn vivo/ 
in vitro
ModelsEffective doses/doses rangeMechanismsToxic effectReferences

Amomum xanthioides Wall. ex BakerZingiberaceaeAqueous ethanolic extractIn vitro 3T3-L1 adipocytes0.02–0.5 mg/mLPRGU, IIAIND[82]

Angelica hirsutiflora Tang S. Liu, C. Y. Chao, and T. I. ChuangUmbelliferaeMethanolic extractIn vivo ICR mice, 10, 30 mg/KgPIEIND [83]
In vitro HIT-T15 cells, human pancreatic islets50–150 µg/mL

Ramulus cinnamomi LauraceaeCinnamaldehyde, benzyl benzoateIn vivo Kun Ming mice1.4 g/KgCOSRND[39]

Cinnamomum cassia (Nees and T. Nees) J. PreslLauraceaeCinnamaldehyde, cinnamyl acetate, cassiosideIn vivo Kun Ming mice700 mg/KgCOSRND[39]

Eucommia ulmoides Oliv.EucommiaceaeLignansIn vivo Kun Ming mice1.4 g/KgCOSRND[39]
Water extractIn vivo C57BL/KsJ-db/db mice1.87 g/KgIHSGND[84]

Daemonorops draco (Willd.) BlumeArecaceaeEthanol extractIn vivo ICR mice1.2 g/KgPIPR, COSRNO [85]
In vitro RIN-m5F cells10–100 µg/mL<200 µg/mL

Zingiber officinale RoscoeZingiberaceaePhenolic gingerolIn vitro L6 rat myoblast5–40 µg/mLPRGUNO[86]

Acanthopanax senticosus (Rupr. and Maxim.) HarmsAraliaceaeHot water extractIn vivo Db/db mice500 mg/KgINGAND [87]
In vitro Caco-2 cells0.03–4 mg/mL
PolysaccharideIn vivo Wistar rats200 mg/KgCOSRND[88]

Ephedra sinica StapfEphedraceaeL-Ephedrine, alkaloidIn vivo BALB/c mice0.0125 mg/mL,PIPRND[89]

Carica papaya L.CaricaceaeAqueous extractIn vivo Wistar rats0.75, 1.5 g/100 mL, PIPR, COSR, IHSGND[90]

Terminalia chebula Retz.CombretaceaeChloroform extractIn vivo SD ratsShort term study, 100, 200, 300 mg/KgPIEIND [91]
Long term study, 300 mg/Kg

Epimedium brevicornumMaxim.BerberidaceaeIcariinIn vivo SD rats80 mg/KgCOSRND[92]

Salvia miltiorrhiza BungeLamiaceaeHydrophilic extractIn vitro HMEC-1 cells, human microvascular endothelial cells10 µg/mLCOSRND[93]

IIAI: CHM increase insulin sensitivity and ameliorate insulin resistance; PIEI: CHM promote insulin secretion and elevate serum insulin levels; INGA: CHM inhibit α-glucosidase activity; PIPR: CHM protect islet β cells and promote their regeneration; IHSG: CHM increase hepatic glycogen content and suppress gluconeogenesis; INSG: CHM inhibit the secretion of glucagon; PRGU: CHM promote the glucose uptake by adipose and muscular tissues. COSR: CHM control oxidative stress response, such as scavenging oxygen radicals, preventing lipid peroxidation, or inhibiting nitric oxide synthesis; RAAR: CHM regulate the activity of aldose reductase; BLIR: CHM block inflammatory response. NO means not toxic. ND means no data available. YES means toxic.

4. Results

We found more than 40 CHM with hypoglycemic effect in ancient works and reviewed the mechanism of CHM lowering blood sugar. We were led to conclude that a number of CHM, including Panax ginseng C. A. Mey., Astragalus membranaceus (Fisch.) Bunge, and Lonicera japonica Thunb., were used in ancient times and also nowadays. In addition, some CHM used for treating DM in ancient works have not been studied for hypoglycemic effect in modern times, such as Lemna minor L., Gardenia jasminoides J. Ellis, Eleocharis dulcis (Burm.f.) Trin. ex Hensch., and Achyranthes bidentata Blume (Figures 1 and 2). These CHM may have potential to become drugs for the treatment of DM by further exploring their hypoglycemic effects. We also found that some foods were used for treatment of DM in ancient times, and their hypoglycemic effects have been confirmed nowadays [15, 16].

The mechanisms by which CHM treat diabetes include the following: (1) CHM increase insulin sensitivity and ameliorate insulin resistance; (2) CHM promote insulin secretion and elevate serum insulin levels; (3) CHM inhibit α-glucosidase activity; (4) CHM protect islet β cells and promote their regeneration; (5) CHM increase hepatic glycogen content and suppress gluconeogenesis; (6) CHM inhibit the secretion of glucagon; (7) CHM promote the glucose uptake by adipose and muscular tissues (Figure 4). Mechanisms of CHM treating diabetic complications include the following: (1) CHM control oxidative stress response, such as scavenging oxygen radicals, preventing lipid peroxidation, or inhibiting nitric oxide synthesis; (2) CHM regulate the activity of aldose reductase; (3) CHM block inflammatory response. Furthermore, CHM hypoglycemic effects are mainly based on IIAI, PIEI, INGA, PIPR, PRGU, and IHSG and fewer CHM are based on INSG.

5. Discussion

5.1. Limitations of Ancient Records and Modern Studies

First, some CHM can alleviate some symptoms of DM such as polydipsia, polyuria, and polyphagia. However, this does not necessarily mean that they are able to lower blood sugar. These drugs include Phragmites australis (Cav.) Trin. ex Steud., Alisma orientale (Sam.) Juz., and Gypsum fibrosum. Second, toxicological studies on CHM were rarely conducted or no information was available on the toxicity of CHM. Fourth, many modern clinical and experimental studies on CHM were methodologically defective, which reduces their reliability and validity. Chen et al. and Li et al.’s results also stated this limitation [17, 18].

In addition, many modern clinical researches tended to focus on curative effects rather than underlying mechanisms. Although molecular biological, immunological, and phytochemical techniques have been widely applied to study the mechanism of CHM treating DM, the nature of many components or extracts was still not very clear.

5.2. Advantages of CHM in the Treatment of DM

Although CHM have many limitations, as aforementioned, the hypoglycemic effects of some CHM were well documented, and some can effectively ameliorate certain clinical symptoms of DM, such as polydipsia, polyuria, and polyphagia. A number of studies have shown that CHM or their extracts used in combination with western medicines work even better for the treatment of DM [19, 20]. For example, Trigonella foenum-graecum L. Saponin given together with sulphonylureas could effectively control the serum glucose, with few side effects, in DM patients whose serum glucose was not well controlled by oral administration of sulphonylureas [21].

5.3. Recommendations for Further Study of CHM for the Treatment of DM

CHM are increasingly used for the treatment of DM primarily because of increased awareness, on the part of patients and doctors, of their advantages, such as effectiveness, natural origin, and safety. However, in order to further extend their scope of application, the limitations of CHM should be avoided. More evidence-based clinical trials should be performed to substantiate the efficacy of CTM prescriptions and crude CHM for the treatment of DM. To confirm the effect of CHM on DM, larger-scale, multicentered, randomized, and controlled clinical trials are needed and statistical methods should be used in all clinical trials. Besides, the mechanisms of CHM and prescriptions should be examined at the molecular and cellular levels by fully taking advantage of the latest techniques, such as biochemical, biological, molecular biological, and immunological methods. Since adverse side effects associated with use of CHM, such as hepatotoxicity, nephrotoxicity and genotoxicity, were reported frequently, it is urgent to conduct toxicological studies on CHM. In order to achieve higher accuracy and better reproducibility, all studies on CHM should be conducted by following well-established and standardized procedures.

6. Conclusion

CHM used to and still play an important role in the treatment of DM in China and great progresses have been made over the last decades. A great many CHM monomer components possess antidiabetes actions. Therefore, it is of great significance to develop novel CHM for the treatment of DM and its complications. The underlying mechanism by which CHM treat DM are complicated and multifactorial and involve multiple organs; studying the effect of active monomer components of CHM might be a good starting point. It is strongly significant to pay close attention to CHM for treatment of DM and its complications.

Conflict of Interests

The authors declare that there is no conflict of interests regarding the publication of this paper.

Acknowledgment

This review was supported by the 42th China Postdoctoral Science Foundation (20070420179).

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