10.3 Diabetes: Sweet Genes
Diabetes is a worldwide growing problem. There are 25.8 million adults and
children in the US that have diabetes that is 8.3 % of the population. Throughout
the world, 347 million people are diagnosed with diabetes and an estimated
3.4 million deaths in 2004 were related to high blood sugar. By the year 2030, the
WHO predicts that worldwide twice as many deaths will be a direct result of
diabetes as in 2005. Diabetes is a major contributor to heart disease and stroke as
well as blindness, kidney failure, and lower limb amputation and is the seventh
leading cause of death in the United States (Dombrowski et al. 2013).
It is well established that diet, even independent of body weight, can influence
the risk of T2D (Esposito et al. 2010; Salas-Salvadó et al. 2011; Dämon et al.
2011). Vegetables and fruits are notable components of diets associated with lower
risk of T2D (Esposito et al. 2010; Salas-Salvadó et al. 2011; Dämon et al. 2011;
McEvoy et al. 2012; Carter et al. 2010). Plant foods are good sources for nutrients
associated with lower T2D risk, such as fiber (Ye et al. 2012), potassium (Chatterjee et al. 2011), and magnesium (Dong et al. 2011), among others.
A recent study demonstrates the chemo-protective effect of a flavanol-containing
foodstuff such as cocoa, which likely plays a role in the protection afforded by
fruits, vegetables, and plant-derived beverages against diseases such as TD2, for
which excess production of reactive oxygen species (ROS) has been implicated as
a causal or contributory factor (Martín et al. 2013). Ins-1E cells, pancreatic beta
cells, treated with a cocoa phenolic extract showed remarkable attenuation of cell
damage after being submitted to stress. Other results suggest that quercetin or
naringenin may protect b-cells from cytokines toxicity by enhancing cell survival
through PI3-kinase pathway, independent of p-p38 MAPK or Inducible Nitric
Oxide (NO) Synthase (iNOS) (Lin et al. 2012).
On the other hand, a polysaccharide extract derived from Triticum Aestivum
Sprout (TASP) stimulates insulin secretion and production in vitro via K
+ channel
closure and calcium influx on the RIN-5F pancreatic b-cell line and rat pancreatic
islets (Lee et al. 2012). TASP significantly increased glucose-induced 45Ca
2+
uptake and proinsulin mRNA expression in rat islets. Apoptosis is the main form
of b-cell death in diabetes. Ginsenoside Rg1 and Rb1 protect b-cells from high
glucose/cytokine-induced pancreatic b-cell apoptosis by inhibiting NO production
and regulating apoptosis-related genes (Chen et al. 2012). Among these genes,
Bax, Fas, and Caspase-3 gene expressions are upregulated by high glucose,
whereas only Bax and Caspase-3 gene expression are elevated by cytokines.
A study showed that diet-induced gene expression of isolated pancreatic islets
from a polygenic mouse model of the metabolic syndrome (Dreja et al. 2010). In
the prediabetic state, 2,109 islet transcripts were differentially regulated ([1.5fold) between diabetogenic high-fat diet (HF) and a diabetes-protective carbohydrate-Free (CHF) diet. Thirty-nine of the identified genes correlated with data from
the Diabetes Genetics Initiative and Wellcome Trust Case Control Consortium
genome-wide scans for TD2. HF diet-induced early changes in gene expression
296
R. Campos-Vega et al.
Diabetes is a worldwide growing problem. There are 25.8 million adults and
children in the US that have diabetes that is 8.3 % of the population. Throughout
the world, 347 million people are diagnosed with diabetes and an estimated
3.4 million deaths in 2004 were related to high blood sugar. By the year 2030, the
WHO predicts that worldwide twice as many deaths will be a direct result of
diabetes as in 2005. Diabetes is a major contributor to heart disease and stroke as
well as blindness, kidney failure, and lower limb amputation and is the seventh
leading cause of death in the United States (Dombrowski et al. 2013).
It is well established that diet, even independent of body weight, can influence
the risk of T2D (Esposito et al. 2010; Salas-Salvadó et al. 2011; Dämon et al.
2011). Vegetables and fruits are notable components of diets associated with lower
risk of T2D (Esposito et al. 2010; Salas-Salvadó et al. 2011; Dämon et al. 2011;
McEvoy et al. 2012; Carter et al. 2010). Plant foods are good sources for nutrients
associated with lower T2D risk, such as fiber (Ye et al. 2012), potassium (Chatterjee et al. 2011), and magnesium (Dong et al. 2011), among others.
A recent study demonstrates the chemo-protective effect of a flavanol-containing
foodstuff such as cocoa, which likely plays a role in the protection afforded by
fruits, vegetables, and plant-derived beverages against diseases such as TD2, for
which excess production of reactive oxygen species (ROS) has been implicated as
a causal or contributory factor (Martín et al. 2013). Ins-1E cells, pancreatic beta
cells, treated with a cocoa phenolic extract showed remarkable attenuation of cell
damage after being submitted to stress. Other results suggest that quercetin or
naringenin may protect b-cells from cytokines toxicity by enhancing cell survival
through PI3-kinase pathway, independent of p-p38 MAPK or Inducible Nitric
Oxide (NO) Synthase (iNOS) (Lin et al. 2012).
On the other hand, a polysaccharide extract derived from Triticum Aestivum
Sprout (TASP) stimulates insulin secretion and production in vitro via K
+ channel
closure and calcium influx on the RIN-5F pancreatic b-cell line and rat pancreatic
islets (Lee et al. 2012). TASP significantly increased glucose-induced 45Ca
2+
uptake and proinsulin mRNA expression in rat islets. Apoptosis is the main form
of b-cell death in diabetes. Ginsenoside Rg1 and Rb1 protect b-cells from high
glucose/cytokine-induced pancreatic b-cell apoptosis by inhibiting NO production
and regulating apoptosis-related genes (Chen et al. 2012). Among these genes,
Bax, Fas, and Caspase-3 gene expressions are upregulated by high glucose,
whereas only Bax and Caspase-3 gene expression are elevated by cytokines.
A study showed that diet-induced gene expression of isolated pancreatic islets
from a polygenic mouse model of the metabolic syndrome (Dreja et al. 2010). In
the prediabetic state, 2,109 islet transcripts were differentially regulated ([1.5fold) between diabetogenic high-fat diet (HF) and a diabetes-protective carbohydrate-Free (CHF) diet. Thirty-nine of the identified genes correlated with data from
the Diabetes Genetics Initiative and Wellcome Trust Case Control Consortium
genome-wide scans for TD2. HF diet-induced early changes in gene expression
296
R. Campos-Vega et al.