Diabetes mellitus type 2 (English: adult-onset diabetes, obesity-related diabetes, non-insulin-

dependent diabetes mellitus, NIDDM) is a type of diabetes mellitus that occurs is not caused by
the ratio of insulin in the blood circulation, but a metabolic disorder caused by mutations in
many genes, [11] including those expressing β cell dysfunction, impaired insulin secretion,
resistance to insulin cells [12] which is caused by the dysfunction of GLUT10 [13] with hormone
resistin cofactors that lead to tissue cells, especially in the liver becomes less sensitive to insulin
[14] as well as RBP4 that suppress glucose uptake by skeletal muscle but increases the secretion
of blood sugar by the liver. [14] Mutations of these genes often occur on chromosome 19 which
is the densest of chromosomes found in humans. [15]

In NIDDM found that high expression of SGLT1, [16] the ratio of RBP4 and resistin hormones
are high, [14] an increase in the metabolic rate of glycogenolysis and gluconeogenesis in the
liver, [14] a decrease in the rate of increase in the rate of oxidation and esterification in the liver.
[17]

NIDDM can also be caused by dyslipidemia [18], lipodystrophy, [14] and the insulin resistance
syndrome.

In the early stages of the disorder appears is reduced insulin sensitivity, characterized by
increased insulin levels in the blood. [Citation needed] Hyperglycemia can be treated with anti-
diabetic drugs that can improve insulin sensitivity or reduce glucose production from the liver,
but the more severe the disease , insulin secretion was decreased, and therapy with insulin is
sometimes needed. [citation needed] There are several theories that mention the exact cause and
mechanism of this resistance, but is known as central obesity predisposing factor for insulin
resistance, in relation to the expenditure of adipokines (its a group of hormones) that damage the
glucose tolerance. [citation needed] Obesity is found in approximately 90% of patients
developed world with a diagnosis of type 2 diabetes. [citation needed] other factors include a
family history of hatching and, although in the last decade has steadily increased begun to affect
teenagers and children. [citation needed]

Type 2 diabetes can occur without any symptoms prior to diagnosis. Type 2 diabetes usually,
initially treated by changes in physical activity (exercise), diet (generally a reduction in
carbohydrate intake), and through weight reduction. These can restore insulin sensitivity, even
when weight loss / load is humble,, for example, around 5 kg (10 to 15 lb), most especially when
it is in abdominal fat deposits. The next step, if necessary,, treatment with oral [[antidiabetic
drugs. [As / When / Because] the production of the hormone insulin is initially unimpaired
treatment, oral (often used in combination) can still be used to improve insulin production (eg,
sulfonylureas) and regulate the release / release that do not fit on glucose by the liver (and
attenuate insulin retaliation to some extent (eg, metformin), and substantially attenuate insulin
retaliation (eg, thiazolidinediones). If this fails, insulin medicine will be required to maintain
normal or near normal glucose levels. a orderly way of life on blood glucose checks
recommended in many cases, and most particularly necessary when taking medication.

A dipeptidyl peptidase 4 inhibitor sitagliptin called, was recently allowed to be used as a

treatment for type 2 diabetes mellitus [19] As the dipeptidyl peptidase 4 inhibitor others,
sitagliptin will open up opportunities for the development of tumors and cancer cells. [20] [21]
A very typical phenotype shown by NIDDM in humans is deficient oxidative metabolism in the
mitochondria [22] in striated muscle. [23] [24] In contrast, tri-iodotironina hormone induces
mitochondrial biogenesis and increase in the synthesis of ATP synthase in complex V, increases
activity of cytochrome c oxidase in complex IV, decrease reactive oxygen species, decrease
oxidative stress, [25] is the hormone melatonin will increase the production of ATP in the
mitochondria and increases the activity of respiratory chain, especially in complex I, III and IV.
[26] Together with insulin, all three of these hormones that regulate a cycle of mitochondrial
oxidative phosphorylation in skeletal muscle. [27] on the other hand, metalotionein which
inhibits the activity of GSK-3beta will reduce the risk of deficiency of heart muscle in people
with diabetes. [28] [29] [30]

Simtoma that occur in NIDDM can be reduced dramatically, followed by a reduction in body
weight after intestinal bypass surgery. It is known as a result of increased secretion of incretin
hormones, but experts have not been able to determine whether this method can provide a cure
for NIDDM with changes in glucose homeostasis. [31]

In traditional therapy, flavonoid hesperidin and naringin-containing compounds, known to cause:

[32]

increase in glucokinase mRNA,

increase in GLUT4 expression in the liver and tissues
peroxisome proliferator gamma perceiving improvement
increase in the ratio of plasma insulin, and leptin protein C [33]
reduction in GLUT2 expression in the liver
decrease in the ratio of plasma fatty acid and triglyceride levels in the liver
decrease in the ratio of plasma and liver cholesterol levels in, among others, by pressing the
3-hydroxy-3-methylglutaryl-coenzyme reductase, acyl-CoA, cholesterol asiltransferase
decrease in fatty acid oxidation in the liver and the activity of carnitine palmitoyl, among
others, by reducing the synthesis of glucose-6 phosphatase dehydrogenase and phosphatidic
fosfohidrolase
increase the rate of glycolysis trajectory and / or decrease the rate of gluconeogenesis
trajectory

being naringin alone, lowered mRNA transcription karboksikinase phosphoenolpyruvate and

glucose-6 phosphatase in the liver.

Hesperidin is an organic compound that is found in many types of citrus fruits, naringin is found
in many types of fruit wines.