associated with increased cell cycle progression, proliferation, and differentiation
of islet cells, and oxidative stress (Table 10.1). In addition, pathway analysis
identified oxidative phosphorylation as the predominant gene set that was significantly upregulated in response to the diabetogenic HF diet. Acacia Polyphenol
(AP) significantly suppressed increases in body weight, plasma glucose, and
insulin in obese diabetic KKAy mice fed HF diet (Ikarashi et al. 2011). AP
increased mRNA expression of adiponectin and adiponectin secretion, suppressed
TNF-a secretion and mRNA expression by white adipocytes, and elevated GLUT4
(mRNA) expression in skeletal muscle in addition to reducing obesity. Another
potential antidiabetic and liver-protective agent, CAPE suppressed hepatic glucose
output by inducing mRNA expression of Glucokinase (Glk) and Pyruvate Kinase
(Pyk) in streptozotocin-induced diabetic rats, while inhibiting phoshoenolpyruvate
carboxykinase in diabetes. CAPE also decreases the harmful effects of diabetes on
the liver of rats (Celik et al. 2009).
A Ginkgo Biloba Extract (GBE) has been associated with diabetes control.
GBE improves glucose metabolism in diabetic rats and reduces the diabetesinduced diaphragm damage. The mechanism of action of the extract may be
related to the promotion of the mRNA expression of GLUT4 in diaphragm and
improvement in the uptake and metabolism of blood glucose (Li et al. 2010).
Berberine, a quaternary ammonium salt found in plants such as Berberis, goldenseal (Hydrastis canadensis), and Coptis chinensis, restores diabetic endothelial
dysfunction through enhanced NO bioavailability by upregulating eNOS (NO
synthase) and suppressing NADPH oxidase expressions in diabetic rats induced by
high-fat diet and streptozotocin (Wang et al. 2009). Also, dietary quercetin (a
flavonoid), alleviates diabetic symptoms and reduces streptozotocin-induced disturbance of hepatic gene expression in mice. Quercetin may improve liver and
pancreas functions by enabling the recovery of cell proliferation through the
inhibition of Cdkn1a expression (Kobori et al. 2009) (Table 10.1). Other study
showed that emodin, bioactive compound extracted from R. palmatum L, one of
the most widely used herbs in Chinese medicine, significantly elevated the mRNA
expression level of PPAR c and regulated the mRNA expressions of LPL, FAT/
CD36, resistin, and FABPs (ap2) in liver and adipocyte tissues (Xue et al. 2010).
A systematic review showed that the improvement of b-cell function and
insulin secretion is possible with antioxidant compounds from antidiabetic plants
(Abdollahi et al. 2012). The most important pathways for the improvement were:
oxidative stress suppression, cytokine-induced impairment, suppression of nuclear
factor NF-jB- a key regulator of endothelial activation, Uncoupling Protein 2
(UCP2), activation, insulin-like activity, and intracellular calcium expression.
Only a limited number of studies report unbiased, genome-wide expression
profiling of pancreatic islets in the course of a diabetogenic dietary intervention in
rodents. Even fewer studies have investigated diabetes-associated global gene
expression profiles in human samples from donors with TD2. However, the
overlap of genes implicated in both adaptation to diabetes-inducing nutritional
factors in rodent studies and genes differentially regulated in TD2 is striking. In
islets, overload of glucose and long-chain fatty acids results in induction of genes
10 Natural Foods as Biosystems to Face Noncommunicable Chronic Diseases
297
of islet cells, and oxidative stress (Table 10.1). In addition, pathway analysis
identified oxidative phosphorylation as the predominant gene set that was significantly upregulated in response to the diabetogenic HF diet. Acacia Polyphenol
(AP) significantly suppressed increases in body weight, plasma glucose, and
insulin in obese diabetic KKAy mice fed HF diet (Ikarashi et al. 2011). AP
increased mRNA expression of adiponectin and adiponectin secretion, suppressed
TNF-a secretion and mRNA expression by white adipocytes, and elevated GLUT4
(mRNA) expression in skeletal muscle in addition to reducing obesity. Another
potential antidiabetic and liver-protective agent, CAPE suppressed hepatic glucose
output by inducing mRNA expression of Glucokinase (Glk) and Pyruvate Kinase
(Pyk) in streptozotocin-induced diabetic rats, while inhibiting phoshoenolpyruvate
carboxykinase in diabetes. CAPE also decreases the harmful effects of diabetes on
the liver of rats (Celik et al. 2009).
A Ginkgo Biloba Extract (GBE) has been associated with diabetes control.
GBE improves glucose metabolism in diabetic rats and reduces the diabetesinduced diaphragm damage. The mechanism of action of the extract may be
related to the promotion of the mRNA expression of GLUT4 in diaphragm and
improvement in the uptake and metabolism of blood glucose (Li et al. 2010).
Berberine, a quaternary ammonium salt found in plants such as Berberis, goldenseal (Hydrastis canadensis), and Coptis chinensis, restores diabetic endothelial
dysfunction through enhanced NO bioavailability by upregulating eNOS (NO
synthase) and suppressing NADPH oxidase expressions in diabetic rats induced by
high-fat diet and streptozotocin (Wang et al. 2009). Also, dietary quercetin (a
flavonoid), alleviates diabetic symptoms and reduces streptozotocin-induced disturbance of hepatic gene expression in mice. Quercetin may improve liver and
pancreas functions by enabling the recovery of cell proliferation through the
inhibition of Cdkn1a expression (Kobori et al. 2009) (Table 10.1). Other study
showed that emodin, bioactive compound extracted from R. palmatum L, one of
the most widely used herbs in Chinese medicine, significantly elevated the mRNA
expression level of PPAR c and regulated the mRNA expressions of LPL, FAT/
CD36, resistin, and FABPs (ap2) in liver and adipocyte tissues (Xue et al. 2010).
A systematic review showed that the improvement of b-cell function and
insulin secretion is possible with antioxidant compounds from antidiabetic plants
(Abdollahi et al. 2012). The most important pathways for the improvement were:
oxidative stress suppression, cytokine-induced impairment, suppression of nuclear
factor NF-jB- a key regulator of endothelial activation, Uncoupling Protein 2
(UCP2), activation, insulin-like activity, and intracellular calcium expression.
Only a limited number of studies report unbiased, genome-wide expression
profiling of pancreatic islets in the course of a diabetogenic dietary intervention in
rodents. Even fewer studies have investigated diabetes-associated global gene
expression profiles in human samples from donors with TD2. However, the
overlap of genes implicated in both adaptation to diabetes-inducing nutritional
factors in rodent studies and genes differentially regulated in TD2 is striking. In
islets, overload of glucose and long-chain fatty acids results in induction of genes
10 Natural Foods as Biosystems to Face Noncommunicable Chronic Diseases
297