Role of Subcutaneous administration of Insulin in Diabetic Neuropathy

You might also like

Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 6

Role of Subcutaneous administration of Insulin in Diabetic

Neuropathy

INTRODUCTION
 Over 50% of patients with diabetes have damage to their
peripheral nervous systems, which is linked to a high degree of
morbidity.

Diabetes patients are at a higher risk of developing Charcot
joints, foot ulcers, and limb amputation due to diabetes
neurological problems, which initially manifest in the distal
extremities and can cause either numbness or persistent pain.

The main goal of the current DN treatment is to relieve
symptoms, and the outcomes are frequently unsatisfactory.

Establishing suitable pharmacological and nonpharmacological


treatments for diabetic neuropathy (DN), a debilitating
consequence of diabetes, requires defining the pathogenic
pathways that lead to DN.

Diabetes causes two main insults. First is the reduction in
insulin signaling, which can be brought on by insulinopenia or
insulin resistance (type 2), is the resultant elevated blood
glucose levels.

 Accordingly, the role of direct insulin singling on sensory


neurons and how disruption of this signaling may be a
contributing factor to DN .
Insulin as a neurotrophic factor in the PNS

 Insulin is a member of the insulin-like super family that includes


Insulin, IGF1, and IGF2.
 A growing body of literature has now established insulin as a
potent neurotrophic factor that appears essential to promoting
proper neuronal function. Insulin receptors are expressed on
both the DRG neuron soma as well as in the peripheral nerve .
 Several reports have indicated that the insulin receptor is
predominantly expressed in small nociceptive neurons.
 TRPV1 co-labeling indicated 25% of all DRG neurons coexpress
TRPV1 and the insulin receptor and that approximately 68% of
TRPV1 positive neurons express the insulin receptor.

AIMS AND OBJECTIVES

 To determine the role of Subcutaneous Administration of Low


dose Insulin Locally ( Intraplantar) in patients with diabetic
neuropathy.

INCLUSION CRITERIA

 All patients diagnosed with Diabetes and peripheral neuropathy


 Age > 18 years and < 80 years.

EXCLUSION CRITERIA
 Patients with foot deformities and ulcers.
 Diabetic nephropathy
 Patients using subcutaneous insulin for treatment
 Age < 18 years and > 80 years.
 Patients with chronic terminal disease like malignancy.

MATERIAL AND METHODS

 It is a observational study . In which effect of local administration


of low dose ( sub hypoglycemic )insulin is seen in patients with
diabetic neuropathy.
 Sample size - 150 patients with diabetic neuropathy.

Investigations required

 FBS and PPBS


 HbA1c
 C peptide levels
 Serum fasting insulin levels
 Serum creatinine and blood urea
 Complete urine examination.
 Biothesiometer
 Patients with diabetes neuropathy are screened and graded by
using Biothesiometer .
 Patients are locally administrated with insulin and are reviewed
at 2, 4 , 8 weeks for improvement.
 They are again with screened with biothesiometer after
3months.

REFERENCES
1. Baura G. D., Foster D. M., Porte D., Jr., Kahn S. E., Bergman R. N., Cobelli C.,
et al.. (1993). Saturable transport of insulin from plasma into the central
nervous system of dogs in vivo. A mechanism for regulated insulin delivery
to the brain. J. Clin. Invest. 92, 1824–1830. 10.1172/JCI116773 [PMC free
article] [PubMed] [CrossRef] [Google Scholar]
2. Bothwell M. (1982). Insulin and somatemedin MSA promote nerve growth
factor-independent neurite formation by cultured chick dorsal root
ganglionic sensory neurons. J. Neurosci. Res. 8, 225–231.
10.1002/jnr.490080212 [PubMed] [CrossRef] [Google Scholar]
3. Brussee V., Cunningham F. A., Zochodne D. W. (2004). Direct insulin
signaling of neurons reverses diabetic neuropathy. Diabetes 53, 1824–
1830. 10.2337/diabetes.53.7.1824 [PubMed] [CrossRef] [Google Scholar]
4. CDC National Diabetes Fact Sheet. (2014). National estimates and general
information on diabetes and prediabetes in the united states (2011),
in Centers for Disease Control and Prevention, 2011, ed C. US Department of
Health and Human Services (Atlanta, GA: CDC, National Diabetes Fact
Sheet; ), 1–12. [Google Scholar]
5. Chalk C., Benstead T. J., Moore F. (2007). Aldose reductase inhibitors for
the treatment of diabetic polyneuropathy. Cochrane Database Syst.
Rev. 2007:CD004572 10.1002/14651858.cd004572.pub2 [PMC free
article] [PubMed] [CrossRef] [Google Scholar]
6. Chen D. K., Frizzi K. E., Guernsey L. S., Ladt K., Mizisin A. P., Calcutt N. A.
(2013). Repeated monitoring of corneal nerves by confocal microscopy as
an index of peripheral neuropathy in type-1 diabetic rodents and the
effects of topical insulin. J. Peripher. Nerv. Syst. 18, 306–315.
10.1111/jns5.12044 [PMC free article] [PubMed] [CrossRef] [Google
Scholar]
7. Cheng Z., Tseng Y., White M. F. (2010). Insulin signaling meets
mitochondria in metabolism. Trends Endocrinol. Metab. 21, 589–598.
10.1016/j.tem.2010.06.005 [PMC free article] [PubMed]
[CrossRef] [Google Scholar]
8. Chiu S. L., Chen C. M., Cline H. T. (2008). Insulin receptor signaling
regulates synapse number, dendritic plasticity, and circuit function in
vivo. Neuron 58, 708–719. 10.1016/j.neuron.2008.04.014 [PMC free
article] [PubMed] [CrossRef]

You might also like