The development of diseases in function of obesity

The obesity favours the development of several diseases, we will give priority to those that result from metabolic disturbances. It is important to say that the excess weight is not the only determining factor, but also how the fat is distributed in the body as I have shown before here on the blog. To remind you:

– Obesity android or apple: accumulation in the central region or the abdominal, being the most dangerous.

– Obesity ginoide or pear: accumulation in the region of the hip.

Diabetes mellitus

As a curiosity, does anyone know what does the word diabetes mellitus?

The first is of Greek origin, meaning siphon it is a system that allows the passage of water from one side to the other, representing the excess thirst and urge to urinate. The second, mellitus of Latin origin meaning “sweetened or honey”, characteristic of the urine of a diabetic person.

Types of diabetes

 Type 1 Diabetes arises from a failure of the pancreas that stops producing insulin, occurs in people with a genetic predisposition. The body starts attacking the pancreas because it didn’t recognize it as a body generating a reaction auto immune. As insulin is the hormone responsible for turning glucose into energy reserve, doses are required daily to maintain the metabolism. It is more frequent in people of age less than 35 years and accounts for only 5% of all diabetes cases.

Type 2 (tipo 2) in addition to the genetic factor has a strong influence of physical inactivity, poor diet and excess weight. Its incidence is higher in people with more than 40 years. Occurs a deficiency in production of insulin by the cells betas, featuring a frame of insulin resistance. It is the main type of diabetes.

We’ll show you some data that show the strong relationship between being obese and have diabetes, remembering that for the obese smokers it is even worse.

  • For every 10% increase in body weight, there is an increase of 2 mg/dl in fasting blood glucose levels.
  • For people with a Body Mass Index (BMI) (kg/m2) above 35, the chances are 93 times in women and 42 in men;
  • Obesity android increases the risk of the occurrence of diabetes mellitus non-insulin dependent on ten times. Around 75% of diabetic patients not dependent on insulin are above the desirable weight.
  • Waist circumference greater than 100 cm can alone elevate the risk of development of diabetes in 3.5 times, even after control for BMI.

Action of insulin on the metabolism of lipids

 Insulin is secreted by beta cells of the islets of the pancreas in response to increased circulating levels of glucose and amino acids after meals. It is a hormone sintetizante (anabolic), reducing the production of glucose by the liver (via decreased gluconeogenesis and glycogenolysis) and increasing the uptake of peripheral glucose, mainly in muscular tissues and adipose.

The adipose tissue acts increasing the demand for insulin, because this reduces the breakdown of fat (como fazer para emagrecer rápido)  and favors the formation of the same. In the obese, is created a resistance to their action, possibly a reduction of insulin receptors or some problem in the transport cell. This generates an increase in the levels of glucose in the blood and consequent hyperinsulinemia. Despite this, the lipogenesis (fat synthesis) is favoured due to the large sensitivity of adipose tissue to insulin.

The lípideos are regulated by a family of transcription factors designated SREBP (sterolregulatoryelement-bindingproteins). SREBPs activate directly the expression of about 30 genes that act in the synthesis and uptake of cholesterol, fatty acid, triglycerides, and phospholipids, as well as of NADPH a cofator indispensable for the synthesis of these molecules. In the liver, three SREBPs regulate the production of lipids. SREBP-1c increases preferentially the transcription of genes involved in the synthesis of fatty acid, among them, the acetyl CoA carboxilase (ACC), which converts acetyl CoA to malonil CoA and fatty acid synthetase (FAS), which converts the malonil CoA to palmitate.

 Insulin stimulates the synthesis of fatty acid in the liver in periods of excess carbohydrates is mediated by the increase of SREBP-1c. In adipocytes the insulin also reduces lipolysis through inhibition of the lipase, hormone sensitive. This enzyme is activated by PKA (protein kinase A). Insulin inhibits the activity of PKA, activating the phosphodiesterase cyclic AMP-specific (PDE3B), which reduces the levels of cyclic AMP in the adipocytes.

This way, you realize that insulin resistance and hyperinsulinemia worsen the problem of diabetes.

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