Diabetes is a very serious disorder of metabolism. This condition occurs when the body can not properly use glucose levels towards energy production. Unhealthy levels of glucose in the blood can lead to long and short-term health complications.

Types of Diabetes Mellitus

Diabetes Type I

A 10% of people with diabetes have Type I.

This is an autoimmune condition where the body itself destroys insulin-producing cells, causing a rapid increase in blood glucose levels.

 

Diabetes Type II

A 90% of people with diabetes have Type II.

In this category, the body either produces insulin that does not work properly, or does not produce enough insulin, so that glucose accumulates in the blood.

 

Complications of Diabetes

Diabetes is associated with a number of complications. These complications are widespread and are due to the chronic increase in blood glucose levels, resulting in damage to the vessels.

 

The resulting complications are grouped into two categories.

 

The category of "microvascular disease"

This category concerns the damage caused to small blood vessels.

Microvascular complications include:

• eye disease, called retinopathy,
• kidney disease, called nephropathy
• nerve damage, called neuropathy

 

The category of "macro-vascular diseases"

This category concerns the damage caused to the arteries

The main macrovascular complications include:

• Accelerated cardiovascular disease resulting in myocardial infarction
• cerebrovascular diseases, which appear as strokes

 

 

Although the underlying etiology remains controversial, diabetes is also associated with myocardial dysfunction, which occurs independently from atherosclerosis. Other chronic complications of diabetes include depression, dementia and sexual dysfunction.

 

With conventional clinical treatment, the risk of major chronic complications in type 1 diabetes, based on the DCCT (Diabetes Control and Complications Cohort) study and the EDIC study, is:

47% for retinopathy,

17% for nephropathy and

14% for cardiovascular disease.

 

For type II diabetes, there are limited data, with significant differences in relative proportions of the various complications among patients.

 

 

Diabetic Nephropathy

Diabetic nephropathy is the main cause of end-stage renal failure. Clinically characterized by the development of proteinuria with a further reduction in the glomerular filtration rate, which lasts for a long time, often over 10-20 years.

 

Nephropathy is also an important risk factor for the development of macrovascular complications, such as heart attacks and strokes. Hypertension and limited glycemic control often precede the onset of diabetic nephropathy. When nephropathy is detected, there is often an increase in blood pressure.

 

The development and progression of nephropathy is extremely complex, given the variety of cellular populations present in the kidney and the different physiological roles of this organ.

 

In fact, in addition to infiltration of toxins by the blood for excretion, it is difficult to name which other functional aspects of the kidney are most affected by diabetics. These functions include the release of hormones, such as erythropoietin, vitamin D activation and the acute control of hypoglycemia, in addition to supporting fluid balance and blood pressure by resorption.

 

High glucose concentrations cause specific cellular effects, which affect various kidney cells, including endothelial cells, smooth muscle cells, mesangial cells, subcellular cells, tubular system cells and collecting duct system and inflammatory cells and myoinoblasts.

 

 

Diabetic Retinopathy

Diabetic retinopathy is characterized by a spectrum of retinal spots and is the main cause of blindness in adults aged 20-74 years.

 

The appearance of these spots includes:

• changes in vascular permeability,
• capillary micro feeds
• capillary degeneration
• excessive formation of new blood vessels (neovascularization)

 

The retina becomes dysfunctional due to the necrosis of certain cells, which changes its electrophysiology and leads to inability to distinguish between the colors.

 

Clinically, diabetic retinopathy is segregated in non-proliferative and proliferative disease.

 

In early stages, hyperglycemia can lead to death and density of the pericia, which helps to change the integrity of the blood vessels in the retina, changing the retinal barrier and vascular permeability.

 

• At first stages of non-proliferative diabetic retinopathy, most people see no difference in vision.

 

Degeneration or obstruction of the retinal capillaries is strongly associated with prognostic deterioration, which is likely to be the result of ischemia followed by subsequent angiogenic release.

 

This promotes the disease in the proliferative phase, where neovascularization as well as the accumulation of fluid in the retina, known as macular edema, contribute to visualization.

 

In more serious cases, there may be bleeding with relative retinal deformity, including the development of a fibro-vascular membrane, which can then lead to retinal detachment.

 

• In Type I Diabetes, the main disorder that threatens vision is manifested by proliferative retinopathy.

 

• Type II diabetes has a higher incidence of macular edema.

 

Diabetic Neuropathy

More than 50% of people with diabetes eventually show neuropathy.

 

Diabetic neuropathy is a syndrome involving both somatic and autonomic peripheral nervous system segregation.

 

However, there is a growing appreciation that even damage to the spinal cord and the upper central nervous system can occur.

 

Additionally, neuropathy is a major factor in reducing the ability to heal a trauma, the occurrence of erectile dysfunction and cardiovascular dysfunction, seen in diabetes.

 

Advanced neuropathy, due to the aggravation of nerve fibers from diabetes, is characterized by sensitivity to vibrations and thermal limits, which lead to a loss of sensory perception.

 

Hyperalgesia, anxiety disorders and allodynia also occur in a 40-50% of patient who experience pain caused from diabetic neuropathy. Pain is also seen in a 10-20% of diabetic individuals who may not show clinical signs of neuropathy but are capable of severely inhibiting quality of life.

 

The size of the neurons is also important. It appears that in diabetes, longer nerve fibers show a faster loss of nerve conduction velocity with loss of their nerve terminals. Therefore, tingling and loss of sensation and reflexes are often seen first on the feet and then go up to affect other areas, especially hands.

 

 

AGEs: Ultimate Sweetening Products and their Participation in the Impact of Diabetes Mellitus

Complications from diabetes mellitus represent clinically defined endpoints that appear to appear as a result of a series of complex intracellular pathways. These pathways can act individually or synergistically to cause adverse effects in multiple organs.

 

Despite the availability of newer and more effective agents for the treatment of diabetes, the various complications of diabetes are still the main cause of morbidity and mortality in these patients.

 

With the increased duration of diabetes, glycemic control is exacerbated, leading to delayed complications.

 

The accumulation of AGEs, formed during periods of hyperglycemia and remaining uncontroversial for many years, may be one of the most important factors that affect metabolic memory.

 

AGEs are a heterogeneous group of chemical entities that appear as a result of a non-enzymatic reaction of glucose with proteins, lipids and nucleic acids.

 

They act directly to cause long-lasting cross-linking of proteins, such as collagen, to promote vascular stiffness and thus alter vascular structure and function.

 

They can also interact with certain receptors to induce intracellular signaling leading to increased oxidative stress and treatment of key proinflammatory and proliferative cytokines.

 

Modification of mitochondrial proteins by AGEs may be irreversible and may lead to decreased mitochondrial function and increased formation of reactive oxygen radicals.

 

Direct inhibition of mitochondrial damage, during adequate glycemic control, helps to improve dysfunction of mitochondrial biogenesis.

 

We conclude that adequate glycemic control, coupled with treatments designed to modulate mitochondrial homeostasis, can help diabetic patients to inhibit further development of complications from diabetes mellitus.