Evaluation of the influence of oral administration of carnosine in combination with vitamin B Complex in preventing the progression of diabetic neuropathy in type 2 diabetes patients.

Diabetic peripheral neuropathy (DPN) is considered the most common chronic complication of diabetes mellitus, with an incidence rate of about 50%.

DPN is a group of clinical syndromes that affects single or combined regions in the nervous system and is considered one of the microvascular complications that affect greatly the quality of life of patients due to pain and frequency of hospitalization.

DPN commonly develops silent without symptoms in the early stages and when symptoms start appearing only a few effective therapies are available and that is what causes significant patient suffering and societal burden.

Those mechanisms of pain and treatment remain challenging and are restricted by variable efficacy and side effects of therapies and intensification of glycemic control remain the cornerstone for the prevention or delay of DPN.

Lately, it has been proven that long-term low-grade inflammation has an important role in DPN pathogenesis. Clinical trials in DPN patients with pain and without pain showed that the DPN with pain group had higher inflammation markers.

In addition, DPN patients with pain had more increased cytokine levels compared with DPN patients without pain. Besides the correlation between abnormalities in nerve fibers and the rise in interleukin (IL)-6 and IL-10.

Moreover, Oxidative stress plays an important role in the development of diabetic neuropathy a reactive oxygen species (ROS) increases the progression of nerve fiber damage and dysfunction.

Those reactive oxygen species are capable of destroying the lipids found in the myelinated structures of nerves resulting in axon loss and disturbance in the microvasculature of the peripheral nervous system.

Antioxidants are available endogenously as a normal defense mechanism of the cell or obtained exogenously from diet and could play an important role in the progression of damage to the neurons in Diabetic neuropathy.

Carnosine, a naturally-occurring dipeptide (β-alanyl-L-histidine) first described in 1900 by Gulewitsch and Amiradzibi, is found predominantly in post-mitotic tissues (e.g. brain and innervated muscle) of vertebrates.

Carnosine is claimed to decrease oxygen-free-radical mediated damage to cellular macromolecules either by chelating divalent cations or scavenging hydroxy radicals with its imidazole moiety. Free-radical damage is not the only process to affects the structure of proteins and nucleic acids.

Furthermore, previous studies proved the neuroprotective action of carnosine with its anti-inflammatory and antioxidant properties.

Moreover, another study highlighted the use of carnosine as a supportive treatment against neurotoxins.

Also, Carnosine has been shown to protect cultured neurons from oxygen-glucose deprivation and to exhibit neuroprotective properties in animal models of global and cerebral ischemia

Inclusion Criteria:

• Type 2 diabetes Patients as per ADA criteria.
• Patients were showing clinical signs of Diabetic neuropathy verified by a neurologist and confirmed by a score ≥7 on the MNSI questionnaire (Michigan Neuropathy Screening Instrument), with abnormal nerve conduction measurement.
• Patients on a regular visit to the clinic.

Exclusion Criteria:

• Patients with neuropathy of non-diabetic origin were excluded.
• Patients with a BMI of 40 kg/m2 or more and those pregnant or breastfeeding were also excluded

intervention clinical trial