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Role ofMedicinal Plants
https://t.me/medicina_free
intheManagement ofDiabetes Mellitus
SarojSinghmura, SouvikBasak, andNilanjanGhosh
Abstract
Since ancient times, cure or prevention of diseases by
medicinal plants was being practiced by indigenous people of different communities around the world through
their traditional approaches. The development of civilization and humankind has shown the path of dening properties of medicinal plants and improvement in dealing
with different diseases by the identication of responsible
molecules. Diabetes mellitus (DM) represents a signicant metabolic disorder of considerable concern. The disruption of insulin action in maintaining glucose
homeostasis arises from elevated blood glucose levels,
which can result from defects in insulin synthesis, secretion, binding to receptors, or increased insulin resistance.
Other risk factors, such as obesity, urbanization, and
genetic mutations, can further contribute to the development of DM. To counter this pathophysiological condition, several marketed remedies are available, but they
limit their uses because of their expensive and several
complications. On the other hand, the management of diabetes mellitus by herbal medicines is less cost-effective
and the complications are also rare.
Keywords
Bioactive phytoconstituents · Glucose metabolism ·
Medicinal plants · Insulin resistance · Diabetes mellitus
S. Singhmura · S. Basak
Dr. B.C. Roy College of Pharmacy and AHS, Durgapur, India
N. Ghosh (*)
Department of Pharmaceutical Technology, Jadavpur University,
Kolkata, India
e-mail: nilanjanghosh.phamacy@jadavpuruniversity.in
1 Introduction
Diabetes mellitus is a persistent metabolic disorder
marked by increased levels of blood glucose resulting
from inadequate insulin production or ineffective utilization of insulin by the body and has become a global health
concern. Globally, over 400 million people are currently
affected by diabetes, and projections suggest this number
may rise to 640 million by the year 2040. The impact of
this disease is staggering, encompassing both public
health expenses for diabetic patient care and the personal
costs associated with severe complications. Approximately
90% of all diabetes cases are type 2 diabetes mellitus
(T2DM) and are characterized by obesity, insulin resistance, and a gradual decline in insulin secretion. Genetic
predisposition, age, obesity, improper dietary habits, and
sedentary lifestyles are among the most signicant factors
contributing to the development of this condition. Thus,
managing diabetes effectively is crucial to prevent complications and improve the quality of life for those living
with the condition. The growing interest in natural and
alternative therapies for diabetes management is a necessity of the time because of the side effects and economic
burden of its management and hence medicinal plants
have emerged as promising candidates in this regard. For
centuries, traditional medicine systems have recognized
the therapeutic potential of various plant species in controlling blood sugar levels and alleviating diabetes-related
symptoms. The role of medicinal plants in managing diabetes mellitus is multifaceted. Within these medicinal
plants, a rich assortment of bioactive compounds, including alkaloids, avonoids, anthraquinone, saponins, glycosides, and carbohydrates, has been identied, exhibiting
remarkable antidiabetic properties. Scientic research has
focused on investigating the mechanisms of action of
these compounds and their potential benets in regulating
glucose metabolism, enhancing insulin sensitivity, and
reducing insulin resistance.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
A. K. Dhara, S. C. Mandal (eds.), Role of Herbal Medicines, https://doi.org/10.1007/978-981-99-7703-1_5
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2 Background: Blood Glucose
Homeostasis andIts Faith inDiabetes
Mellitus
Insulin maintains blood glucose homeostasis by taking into
the cells, thus its level is maintained. If this regulation is disturbed, it results in a hyperglycemic state, and if not regulated, prolonged exposure may lead to chronic complications
affecting the renal, neurological, gastrointestinal, genitourinary, cardiovascular system, and lower extremity [1]. In individuals without diabetes, the blood glucose concentration is
meticulously controlled to provide a constant energy source
for various tissues and organs. Insulin and glucagon, the primary hormones responsible for this equilibrium, are both
secreted by the pancreas' β cells. Their release is triggered by
a complex interplay of metabolic, hormonal, neuronal, and
pharmacological factors, working through interconnected
intracellular signaling pathways.
2.1 Pathways ofInsulin Secretion
The secretion of insulin is a highly controlled process aimed
at maintaining stable blood glucose levels during fasting and
feeding periods. This delicate regulation relies on the orchestrated interaction between glucose and non-nutrient secretagogues, such as neurotransmitters and hormones.
2.1.1 Pathway ofInsulin Secretion Induced by
Glucose Stimulation
The homeostatic blood glucose level is upheld by insulin
released by the beta (β) cells within the pancreatic islets of
Langerhans. Insulin plays a pivotal role in governing the
body's metabolism of carbohydrates, proteins, and fats. Its
main function involves facilitating the uptake of carbohydrates, predominantly glucose, from the bloodstream into
skeletal muscle, adipose tissue, and the liver. When foods
containing carbohydrates are ingested, enzymatic processes
trigger a rise in blood glucose levels, which is detected by
beta (β) cells (Fig.1). Subsequently, these cells take up glucose from the bloodstream via glucose transporters (GLUTs)
and engage in glycolysis, leading to an increase in ATP production [2, 3]. Elevated levels of this leads to the suppression
of the cell's K
channels. [4, 5]. K
ATP
channels are made up
ATP
of two different proteins: sulfonylurea receptor (SUR) subunits and pore-forming (Kir6.x) subunits (Figs. 2 and 3).
Channel activity is stimulated by Mg-nucleotide binding/
hydrolysis at the nucleotide-binding domains (NBD1 and
NBD2) of SUR subunit [6]. The closure of the pore in Kir6.2
is induced by the binding of ATP or ADP, and this effect does
not depend on Mg2+. Consequently, the closure of KATP
channels results in depolarization and subsequent activation
of L-type Ca2+ channels. This activation permits an inux of
Ca2+ into the cell [5, 7–9], followed by exocytotic release of
insulin [10]. This exocytosis of insulin from β-cells is rapid,
taking place within the rst 5–10 min, commonly known as
the rst phase of secretion. Following this, a sustained
release, known as the second phase secretion, occurs. The
signicance of the second phase lies in its potential to
become quantitatively signicant, as it can be maintained for
several hours in cases where elevated blood glucose levels
persist [11]. In addition to the insulin secretion mechanism
mentioned above, it is important to acknowledge that glucose can stimulate insulin release through other means.
Notably, any alterations in the channels present in β-cells
that impact membrane potential could also inuence the
movement of Ca2+ into the cytosol, thereby inuencing insulin secretion [12–14].
Fig. 1 Insulin secretion
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Fig. 2 K
Fig. 3 K
channel (stimulate)
ATP
channel (closed)
ATP
2.2 Gut Hormone Pathway
Incretins are gastrointestinal hormones released in response
to food intake. Glucagon-like peptide-1 (GLP-1) is secreted
from enteroendocrine L cells, which are distributed throughout the small and large intestines. Similarly, glucosedependent insulinotropic polypeptide (GIP) is secreted from
enteroendocrine K cells in the duodenum and jejunum. Once
released, these incretins bind to their specic G-proteincoupled receptors, leading to the activation of adenylate
cyclase and subsequent elevation of intracellular cAMP levels [15], followed by activation of PKA (protein kinase A)
and cAMP-binding proteins referred to as cAMP-regulated
guanine nucleotide exchange factors (cAMP GEFs), also
known as Epac2 (Exchange protein directly activated by
cAMP 2) or cAMP-GEFII [16]. PKA activation is believed
to facilitate exocytotic release of insulin [17–19].
Dipeptidyl peptidase-4 (DPP4) (Fig.4) is an extensively
distributed enzyme that exerts its actions through both a
membrane-anchored transmembrane molecule and a soluble
circulating protein [15]. DPP4 plays a signicant role in glucose homeostasis. By breaking down these incretin hormones, DPP4 reduces their ability to promote insulin
secretion, leading to decreased insulin release and impaired
glucose clearance from the bloodstream. Overall, the regulatory role of DPP4in incretin hormone metabolism and glucose homeostasis highlights its signicance in maintaining
proper blood glucose levels in the body.
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Fig. 4 Dipeptidyl peptidase-4
(DPP-4) enzyme
S. Singhmura et al.
3 Regulation Glucose Level
3.1 Enzymatic Action
Carbohydrates constitute the primary components of the
typical human diet. Among its major forms, starch and
sucrose contribute around 70–80% of the body’s energy
requirements. The digestion of carbohydrates begins in the
mouth and continues in the small intestine, resulting in the
production of glucose. This glucose is then absorbed into the
bloodstream through the enzymatic action within the intestinal walls and subsequently transported to various body parts,
facilitated by the liver. Polysaccharides (starch) is converted
into maltose, sucrose, and lactose (Disaccharides) and then
nally into glucose, the main digested product, along with
small amount of fructose and galactose (monosaccharides).
The breakdown of starch initially occurs through α-amylase,
an enzyme presents in saliva and pancreatic juices, which
converts it into oligosaccharides. Subsequently, a membranebound enzyme called α-glucosidase, found in the small
intestine's epithelium, catalyzes the cleavage of glucose from
disaccharides and oligosaccharides, leading to postprandial
hyperglycemia. Due to this process, inhibiting α-amylase
and glucosidase can be an effective treatment for diabetes.
By doing so, the absorption of glucose is delayed, which can
be benecial for individuals with impaired insulin response
or production. In hepatocytes, glycolysis regulates hepatic
glucose levels. Pancreatic β cells couple glycolysis with
glucose- stimulated insulin secretion. Adipocytes utilize gly-
colysis to produce metabolites for lipogenesis and divert
excessive fatty acids away from oxidation, reducing oxidative stress. In a proinammatory state, adipocytes release
prohyperglycemic factors, leading to hyperglycemia and
insulin resistance. In hypothalamic neurons, glycolysis is
involved in nutrient sensing, which inuences feeding control. Dysregulation of glycolysis can contribute to the development of diabetes.
An imbalance in glucose-6-phosphatase activity can lead
to hyperglycemia in diabetes. Aldose reductase (AR), a cytosolic enzyme, normally performs several essential functions,
including detoxifying harmful aldehydes in extrahepatic tissues, producing fructose for sperm, maintaining osmoregulatory balance in the kidney, and reducing steroids and
catecholamines. However, under certain conditions, AR catalyzes the NADPH-dependent reduction of glucose to sorbitol in the polyol pathway, resulting in an overproduction of
reactive oxygen species (ROS). This increased ROS production can contribute to oxidative stress and other detrimental
effects, potentially exacerbating the complications of diabetes [20]. Converted sorbitol poorly penetrates membranes,
and thus if blood glucose rises, it causes intracellular accumulation along with its metabolites fructose, which creates
osmotic swelling and cell dysfunction [21]. Overuse of
polyol metabolism may cause hyperglycemia, sorbitoland
osmotic buildup,which can all contribute to cataract development. [22–24]. Protein Tyrosine Phosphatase 1B (PTP1B)
is a phosphatase situated on the cytoplasmic side of the endoplasmic reticulum (ER) [25]. Expressed in various tissues,
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including skeletal muscle, liver, adipose tissue, and brain,
Protein Tyrosine Phosphatase 1B (PTP1B) plays a role in
negatively regulating multiple cellular pathways, such as the
response to insulin or endothelial nitric oxide (NO) production [17]. It functions as an essential enzyme in the dephosphorylation of tyrosine (Tyr)-phosphorylated proteins,
making it a key player in the dephosphorylation of the insulin receptor (IR) and its downstream signaling components
[25]. PTP1B has been identied as a key enzyme responsible
for the dephosphorylation of both IR and its downstream signaling component, IRS-1. Disruptions in this pathway can
lead to diverse metabolic disorders, including insulin resistance and type 2 diabetes.
3.2 Advance Glycation End Products
The accumulation of advanced glycation end products
(AGEs) arises from the reaction between carbonyl groups of
reducing sugars and amino groups of proteins, lipids, and
nucleic acids. This cellular dysregulation occurs in diabetes,
leading to various complications such as cardiomyopathy,
neuropathy, retinopathy, and nephropathy, as well as contributing to atherosclerosis and aging. The presence of AGEs
inuences the expression of genes, intracellular signals, and
the release of proinammatory molecules and reactive oxygen species (ROS), further exacerbating the impact on cellular function and contributing to the development of diabetic
complications and other age-related diseases.
3.3 Oxidative Stress
Hyperglycemia can initiate tissue damage through ve signicant mechanisms, all stemming from a single upstream
event: mitochondrial overproduction of reactive oxygen species (ROS) [26].
1. Increased formation of AGEs: Elevated ROS levels in the
mitochondria can lead to increased formation of AGEs.
These harmful compounds can accumulate in tissues,
causing oxidative stress, inammation, and damage to
proteins, lipids, and DNA [27].
2. Activation of Protein Kinase C (PKC): Hyperglycemiainduced ROS production which can activate certain
enzymes, such as PKC. Overactivated PKC can further
promote inammation, disrupt cell signaling pathways,
and contribute to tissue damage.
3. Increased polyol pathway activity: Mitochondrial-derived
ROS can enhance the activity of the polyol pathway, lead-
ing to the accumulation of sorbitol in tissues. This can
cause osmotic stress and damage to nerve cells, blood
vessels, and other structures [28].
4. Altered cellular metabolism and mitochondrial dysfunction: High levels of ROS can disrupt cellular metabolism
and lead to mitochondrial dysfunction. Impaired mitochondria affect the production of ATP, causing energy
depletion and contributing to cellular damage [29].
5. Increased expression of the receptor for advanced glycation end products (RAGE). RAGE is a cell surface receptor that binds to AGEs formed as a result of prolonged
exposure to high glucose levels. When blood glucose levels are elevated, the formation of AGEs is increased.
These AGEs can bind to RAGE on the cell surface, leading to several detrimental effects [30]. Antioxidant ther-
apy in diabetes involves the modulation of various cellular
processes affected by oxidative stress and it can be
achieved by neutralization of Reactive Oxygen Species
(ROS). Antioxidants directly scavenge and neutralize
reactive oxygen species (ROS) generated during oxidative stress. Restoration of antioxidant enzymes by natural
antioxidants can help restore the activity of endogenous
antioxidant enzymes, such as superoxide dismutase
(SOD), catalase, and glutathione peroxidase. These
enzymes play a crucial role in neutralizing ROS and
maintaining cellular redox balance. Antioxidant therapy
can enhance the activity of these enzymes, further bolstering the cellular defense against oxidative stress.
Moreover, it can be done by inhibition of advanced glycation end products (AGEs) formation. Some antioxidants,
such as alpha-lipoic acid, have been shown to inhibit the
formation of AGEs. AGEs are harmful compounds that
form when glucose reacts with proteins, and they contribute to tissue damage and diabetic complications. By
reducing AGEs formation, antioxidants can help mitigate
their detrimental effects on tissues. Antioxidants can further modulate inammatory pathways by reducing the
expression of pro-inammatory molecules, such as cytokines and adhesion molecules. By suppressing inammation, antioxidants can help protect tissues from
inammatory damage seen in diabetes-related complications. Antioxidant can improve mitochondrial function to
reduce oxidative damage within these vital cellular organelles. Improving mitochondrial function contributes to
overall cellular health and energy production and
improves insulin sensitivity and glucose uptake in cells.
By enhancing insulin signaling pathways, antioxidants
may contribute to better glucose regulation in diabetes
[31].
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4 Antidiabetic Phytoconstituents
andTheir Mode ofAction (Fig.5)
Phytoconstituents, or phytochemicals, are natural chemical
compounds that naturally occur in plants. These compounds
play a vital role in the biological activities of plants and are
responsible for their diverse medicinal properties.
Researchers are actively isolating various phytoconstituents
and exploring their potential to develop strategies for managing diabetes mellitus. Isolated phytoconstituents can be classied into several classes based on their chemical structures
and properties, such as alkaloids, avonoids, anthraquinones,
glycosides, saponins, coumarins, and more. This categorization helps in better understanding and utilizing the diverse
therapeutic potentials of these plant-derived compounds in
the management of diabetes and related conditions (Tables 1
and 2).
4.1 Alkaloids
Among the prominent natural product categories, alkaloids
are extensively isolated from medicinal plants and have demonstrated the ability to regulate glucose metabolism in animal models. This research is instrumental in comprehending
and developing strategies for managing diabetes mellitus and
its complications. Isolated alkaloids and their derivatives
have exhibited various modes of antidiabetic activity. These
include enhanced insulin secretion, improved digestion and
absorption of carbohydrates, increased liver glycogen, regeneration of β-cells, inhibition of α-glucosidase, elevated glucose transporter concentration, and inhibition of digestive
enzymes. These diverse mechanisms underscore the potential of alkaloids as valuable resources for the development of
novel treatments in the realm of diabetes management.
4.1.1 Inhibition ofEnzymes
Secondary metabolites isolated from medicinal plants can
inhibit digestive enzymes (Sect. 3.1) and thereby help lower
postprandial blood glucose levels [90]. These compounds
prevent the formation of enzyme-substrate complexes, leading to reduced enzyme activity. For example, carbazole alkaloids from Murraya koenigii L.Spreng (Table2) demonstrate
α-glucosidase inhibition, and mahanimbine exhibits
α-amylase and α-glucosidase inhibitory effects, potentially
benecial in managing diabetes-associated cardiovascular
complications [90]. Several other alkaloids have been found
to effectively stimulate glucose uptake in skeletal muscles,
both insulin-dependent and insulin-independent, such as
O-methylmurrayamine A [48], koenidine [75], mahanimbine
[91], and murrayazoline are found to be effectively stimulating glucose uptake in skeletal muscles (measured in
L6-GLUT4myc myotubes). These carbazole alkaloids
increase in the surface GLUT4myc level [92]. Allylpropyl
disulde isolated from Allium sativumis is involved in glycogen synthesis and insulin secretion. Adhatoda vasica (Nees.)
isolated alkaloids like quinazoline, vasicine, and vasicinol
have shown to inhibit rat intestinal α-glucosidase competitively [32]. Palmatine is a bioactive protoberberine alkaloid,
which was isolated from Coscinium fenestratum stem extract
that has effective alpha-amylase, alpha-glucosidase, and
DPP-IV inhibitor activity, which may be helpful to reduce
the postprandial glucose level [77]. Oriciopsis glaberrima
showed an α-glucosidase inhibitory activity due to
Oriciacridone C, 1,3,5-trihydroxy-4-(c,c-dimethylallyl)acridone and oriciacridone F [93]. Piper umbellatum shows
the α-glucosidase inhibitory activity due to the presence of
three alkaloid piperumbellactam A, B, and C found in the
fraction of the extract from the branches of the plant [94].
Indole alkaloids vindogentianine obtained from leaf extract
in Catharanthus roseus (L.) Gis are able to inhibit both the
Fig. 5 Mode of action of phytoconstituents in the management of diabetes mellitus
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