Obesity And Type 2 Diabetes-How To Overcome it

Obesity And Type 2 Diabetes-The prevalence of obesity and type 2 diabetes mellitus is rising rapidly around the world. About 60% of those who suffer the obes diabetes mellitus type 2. The greater body mass index (IMT) the greater the risk of suffering from diabetes mellitus type2. 

obesity and type 2 diabetes

On the contrary in people with diabetes mellitus type 2 in the United States ,approximately 90.0% had obes and power more (overweight). The results of epidemiological studies in developed countries pointed out that the increasing prevalence of obes in line with the increasing prevalence of diabetes mellitus type 2.

Wannamethee, dkk2 in the United Kingdom to monitor as many as 6916 men middle age for 12 years. From the results of monitoring studies found that the risk of the occurrence of type 2 diabetes mellitus is increasing significantly and progressively in line with increasing body mass index and the length is suffering more power or obes(Figure 1).

The results of these epidemiological studies prove that there is a tight relationship between obesity and diabetes mellitus type 2. Obesity needs to distinguish between a central or visceral obesity and obesity peripheral. From the results of epidemiological studies proved that the Association of obesity and type 2 diabetes mellitus is more apparent in those with obesity. Inspection results with CT-scan of abdominal visceral fat showed that contribute towards the onset of insulin resistance. Although fat is a major Predictor of visceral onset insulin resistance, it seems the relationship not found in those who are normal weight.

Therefore, it can be inferred that the relationship of visceral fat and insulin resistance occurs only on the circumstances in which such excessive visceral fat tissue in people with obes. This article will discuss about the pathophysiology of the onset of type 2 diabetes mellitus in obesity and management

The RELATIONSHIP of OBESITY and type 2 DIABETES MELLITUS

obesity and type 2 diabetes

Diabetes mellitus type 2 occurs by two main disorders ,namely pancreatic beta cellsseptal so that the release of insulin is reduced, and the presence of insulin resistance. In General, most experts agree that diabetes mellitus type 2 begins with the presence of insulin resistance, then the following reduced release of insulin. In people with obes also found the presence of insulin resistance. 

There are allegations that sufferers of diabetes mellitus type 2 starts with a normal body weight, then becoming obes with insulin resistance and ended up with diabetes mellitus type 2. In General, sufferers of diabetes mellitus with typical complaints that come to the clinic have already found good insulin resistance as well as pancreatic beta cells septal.

Fatty tissue has two functions as storage of fat in the form of triglycerides, and as an organ of the endocrine. Fat cells produce a variety of hormones, also called adipositokin (adipokine) leptin, tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), Resistin, and adiponektin. These hormones also play a role in the onset of insulin resistance. In Figure 2  shown the relationship of fatty tissue with insulin resistance

 The role of free fatty acids

On those who are obese or type 2 diabetes mellitus have always found the levels of free fatty acids. Increased free fatty acids on their fat and diabetes mellitus type 2 is caused by increasing the breakdown of triglycerides (the process of lipolysis) in fatty tissues especially in visceral. Increasing lipolysis allegedly associated with increased activity of sympathetic dystrophy of the nervous system. Visceral fat is known as sensitive to stimulation of nerves sympathetic dystrophy so visceral fat cell metabolism is very active. High free fatty acids in plasma were cast against the onset of insulin resistance both on the muscles, liver, and pancreas (Figure 2).

Muscle

In the year 1963 Randle posited the theory that in circumstances where the increaseof free fatty acids in the blood will be followed by increasing free fatty acid ambilanby muscle tissue. In normal circumstances the muscle will use glucose (glucose oxidation) to produce energy. Thus the oxidation of fatty acids in muscle is increased, this will inhibit the glucose by muscle ambilan so there was hiperglikemi (Figure 3A).

Hearts

The same situation occurs in the liver, where the heart will accommodate most of the free fatty acids and become material for the process of gluconeogenesis and VLDLsynthesis. With increased gluconeogenesis, fasting plasma glucose is increased then there was hiperglikemi. State of hiperglikemi this fast will result in insulin resistancein the liver (Figure 3B)

 The pancreas

The mechanism of the "damage" the pancreas on obesity is unclear. It is thought that high free fatty acids will result in the occurrence of excessive trigliserid deposit onthe pancreas, and the beta cells will lead to the occurrence of the damage to the beta cells of the pancreas.

A. Combustion free fatty acids increases the amount of Acetyl CoA, Acetyl CoA overload will hamper the enzyme heksokinase which is an enzyme important to change the oxidation of glucose into glucose-6-phosphate (G-6-P). To improve ambilan glucose, muscle cells need more insulin so glucose can enter into muscle cells, or in other words will occur insulin resistance

B. increased levels of fatty acids in plasma causes the distribution through the portal system to the liver overload so that more fatty acids are oxidized and produce Acetyl CoA. Acetyl CoA to activate the enzyme pyruvate in the liver karboksilase which acts to change glucose into pyruvic acid on the process of gluconeogenesis, thereby finally happening increased production and release of glucose liver. Increased gluconeogenesis work barriers resulted in the liver, insulin or insulin resistance arises.

 The role of adipositokin

A recent study proves that adipositokin (adipokin), which is produced by fat cells play a role in various metabolic processes and the onset of insulin resistance. Leptin, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and improve work resistin resistesi insulin, rather adiponektin work improves insulin sensitivity.

Leptin

Leptin levels in plasma increases with increasing body weight. Leptin works at the Central and peripheral nervous system. The role of leptin against the onset of insulin resistance is unclear. Research on rats, leptin inhibits phosphorylation of insulin receptor substrate-1 (IRS) which consequently impedes ambilan glucose. In contrast, other studies in animals with diabetes obes and leptin, delivery increase insulin sensitivity. Similar things are also reported human studies.

Tumor necrosis factor-alpha

Same with leptin and free fatty acid, plasma TNF-alpha levels increased with increasing weight, and plays a role in the mechanism of peripheral insulin resistance. However, on human levels of TNF-alpha in circulation very little to inhibit insulin work on muscle tissue. Alleged work of TNF-alpha more parakrin than the endocrine, or by other factors, such as free fatty acids, as TNF-alpha stimulate lipolysis. Adipose tissue in rats and humans, TNF-alpha is expressed in excess so that interfere with insulin signaling in the phosphorylation of IRS-1 consequently hampered and suppress the expression of glucose transporter (GLUT)-4.

Interleukin-6

As a proinflamasi protein secreted by adipose tissue, IL-6 also increased with increasing body weight. In humans, the IL-6 spur the  release of glucagon and cortisol and increases gluconeogenesis. Bastard, et al. found that sufferers of diabetes mellitus that obes are more resistant to insulin, the levels of IL-6, TNF-alpha and leptin increased compared to controls not the diabetes mellitus sufferer obes. The role of IL-6 on insulin resistance is suspected through (adiposity), are not directly related to the work of insulin. It is reported by Vozarova, et al. which found that the levels of IL-6 have a correlation with body fat percentage, but there is no correlation with insulin sensitivity at the Pima Indians.

 Resistin

Lazar, et al found a signalling molecule secreted by the deposit and was named resistin. Increased levels of resistin in mice obes induced obes and overeating due to genetics, and reduced by administering anti diabetic drugs agonis peroxisome proliferator-activator receptor (PPAR), such as rosiglitazone.

Adiponektin

Adiponektin peptide hormones are mainly generated by adiposit. Compared with other adipositokin, adiponektin the highest levels in circulation. Adiponektin has an effect contrary to the other adipositokin, namely, preventing the onset of insulin resistance and diabetes mellitus type 2. Weyer et al, reported levels of adiponektin on white people and Indians Pima decreases. Adiponektin levels also correlated with insulin sensitivity, and conversely diminished by increasingly poor glucose tolerance. Other studies in humans, levels of adiponektin increases with the weight loss and the granting of agonis PPAR, rosiglitazone. Work adiponektin allegedly with spur expression genes that regulate the metabolism of fat in the muscle tissue, i.e., CD36, acyl co-enzyme A (CoA) oxidase, and uncoupling protein (UCP)-2 which will improve the efficiency of the transport of fatty acids, and fat burning termogenesis.

MANAGEMENT

obesity and type 2 diabetes

Management on every sufferer of diabetes mellitus treatment consist of a non-medical nutrition therapy i.e. Pharmacology term (planning to eat), sports, education, and the use of drugs to lower blood glucose levels. Specifically for sufferers of type 2diabetes mellitus in non-obese treatment Pharmacology term is very important, because of the weight reduction can only be achieved with medical nutrition therapy and improve body activity/sport. It has been proven that with increasing weight > 10% of initial weight will increase the risk of diabetes mellitus. In contrast with the weight loss diabetics mellitus fat can improve the situation of glucose intolerance.

Management non-Pharmacology term

Non treatment Pharmacology term indeed became the main goal of diabetes mellitus in obese, non-therapeutic Pharmacology term unfortunately it doesn't always work, even more often fail. Therefore, some efforts have sought to keep trying to lose weight sufferers of diabetes mellitus type 2 are obese, with the addition of the antiobesity drugs such as orlistat and sibutramin. Because diabetics mellitus fat is often accompanied by a variety of other metabolic disorders like insulin resistance/hiperinsulinemi, high levels of cholesterol-low accompanied trigliserid HDL and hypertension, by itself treatment in diabetics mellitus fat must be taken into account all of these factors (Figure 4)

Management farmokologik 

Oral hypoglycemic drugs

On a currently marketed as much as five types of oral hypoglycemic drugs, namely sulfonilurea, non-sulfonilurea secretogogue (repaglinid, natiglinid), biguanid, alpha glucosidase inhibitors (akarbose), and thiazolidinedion (pioglitazon, rosiglitazon). Oral hypoglycemic drugs in the election for diabetes mellitus type 2 fat always to be aware of the side effect of increasing the levels of plasma insulin, and increasing weight. The thiazolidinedion, metformin, akarbose and repaglinid are recommended for obese type 2 diabetes mellitus. In certain circumstances the combination treatment needs to be done in addition to single lowers Metformin blood glucose levels also lose weight, therefore it is highly recommended in people with diabetes mellitus type2 fat. 

The thiazolidinedion is very good for sufferers of diabetes mellitus type 2 are obese due to improve insulin sensitivity in the network, but can sometimes raise the weight. At the moment it has marketed the drug combination in a single tablet likeGlucovance (metformin-glibenklamid) and Avandamet (metformin – rosiglitazon). Both of these drugs give  good results in people with diabetes mellitus type 2 are obese, by not raising the weight

Medications associated with cardiovascular risk factors

Because of the prevalence of hypertension, dislipidemi is very high in people with diabetes mellitus, while targets to be achieved very tight then drugs related to cardiovascular risk factors such as drug antihipertensi, hipolipidemik almost routinely given.For the drug antihipertensi for levels of creatinin in normal limits, the first choice is the ACE-inhibitors. Specially when it's been discovered the existence of mikroalbuminuri then the ACE-inhibitors can prevent diabetic nephropathy perlangsungan worse. The Statins to date is still the first choice for diabetic dislipidemi in people with diabetes mellitus type 2, except in those with high levels of trigliserid i.e. > 400 mg/dlthen the fibrat precedence.

The research of the Heart Protection Study using simvastatin 40 mg/day concluded that those with LDL-cholesterol levels < 100 mg/dl may still provide benefits prevention of cardiovascular complications. The American Diabetes Association recommends administering aspirin routinely in people with type 2 diabetes mellitus who > 30 years. It can therefore be concluded that the majority of sufferers of diabetes mellitus type 2 will receive preventative medicine for cardiovascular events.

Anti obesity drug 

Anti obesity drugs such as orlistat and sibutramin, greatly help to lose weight in fat sufferers. The medications in addition to providing weight reduction, it can also provide repair serum lipid profile such as lowering LDL-cholesterol levels and triglycerides, and raise HDL-cholesterol levels. Excellent results in weight can be lowered by 10%of initial weight.

Read also:Type 2 Diabetes Symptoms, Causes, And Treatment

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