Glucose sticks to the haemoglobin to make a 'glycosylated haemoglobin' molecule, called haemoglobin A1C or HbA1C
Wild S, Roglic G, Green A, Sicree R, King H (2004). "Global prevalence of diabetes: Estimates for the year 2000 and projections for 2030". Diabetes Care 27 (5): 1047–53.doi:10.2337/diacare.27.5.1047. PMID 15111519.Williams textbook of endocrinology (12th ed.). Philadelphia: Elsevier/Saunders. pp. 1371–1435. ISBN 978-1-4377-0324-5.
Critical nodes form an important part of the signalling network that functions downstream of the insulin receptor (IR) (black arrows) and the insulin growth factor-1 receptor (IGF1R) (blue arrows). Signalling pathways that are activated by cytokines such as tumour necrosis factor-α (TNFα), interleukin-6 (IL-6), and leptin interfere with insulin signalling through crosstalk (orange and red arrows). Three important nodes in the insulin pathway are the IR, the IR substrates (IRS) 1–4 (light blue box), the phosphatidylinositol 3-kinase (PI3K)with its several regulatory and catalytic subunits (light green box), and the three AKT/protein kinase B (PKB) isoforms (pink box). Downstream or intermediate effectors, as well as modulators, of these critical nodes include atypical protein kinase C (aPKC), Akt substrate of 160 kDa (AS160), Cas-Br-M (murine) ecotropic retroviral transforming sequence homologue (Cbl), Cbl-associated protein (CAP), cell-division cycle 42 (CDC42), extracellular signal-regulated kinase 1 and 2 (ERK1 and ERK2), forkhead box O1 (FOXO1), glycogen synthase kinase 3 (GSK3), Janus kinase (JAK), c-Jun-N-terminal kinase (JNK), mammalian target of rapamycin (mTOR), p90 ribosomal protein S6 kinase (p90RSK), phosphoinositide-dependent kinase 1 and 2 (PDK1 and 2), phosphatase and tensin homologue (PTEN), protein tyrosine phosphatase-1B (PTP1B), Ras, Rac, Srchomology-2-containing protein (Shc), suppressor of cytokine signalling (SOCS), signal transducer and activator of transcription (STAT), and Ras homologue gene family, member Q (ARHQ; also called TC10). Dashed arrows represent an activation process with less intensity.
Rhodes, C.J., Shoelson, S., and Halban, P.A. (2005). Insulin Biosynthesis,Processing, and Chemistry. In Joslin’s Diabetes Mellitus, C.R. Kahn, G.C.Weir, G.L. King, A.M. Jacobson, A.C. Moses, and R.J. Smith, eds. (Boston:Joslin Diabetes Center), pp. 65–82
Diabetes types and treatment
Types & Treatments
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Diabetes mellitus, or simply diabetes, is a
group of metabolic diseases in which a
person has high blood sugar, either
1. The pancreas does not produce enough
2. Cells do not respond to the insulin that is
This high blood sugar produces the classical
symptoms of –
Polyuria (frequent urination)
polyphagia (increased hunger).
Type 1 Diabetes mellitus
Characterized by loss of the insulinproducing beta cells of the islets of
Langerhans in the pancreas, leading to
immune-mediated or idiopathic. The majority
of type 1 diabetes is of the immunemediated nature, in which beta cell loss is a
T-cell mediated autoimmune attack.
There is no known preventive measure
against type 1 diabetes. Most affected people
are otherwise healthy and of a healthy weight
when onset occurs.
Type 1 diabetes can affect children or adults,
but was traditionally termed "juvenile
diabetes" because a majority of these
diabetes cases were in children.
Type 2 Diabetes Mellitus
Type 2 diabetes is a condition where the body is
insulin deficient or has a resistance to the action
Characterized by insulin resistance, which may
be combined with relatively reduced insulin
The defective responsiveness of body tissues to
insulin is believed to involve the insulin receptor.
However, the specific defects are not known.
Diabetes mellitus cases due to a known
defect are classified separately. Type 2
diabetes is the most common type.
In the early stage of type 2, the predominant
abnormality is reduced insulin sensitivity. At
this stage, hyperglycemia can be reversed by
a variety of measures and medications that
improve insulin sensitivity or reduce glucose
production by the liver.
Besides above mentioned types there are
some other also which occurs at certain
( Latent autoimmune diabetes of adults)
Diabetes Nutrition and
A total of 192 diabetic subjects attending
four centres (HCSC, CSCH, CPH, and
HGA) between 1993 and 2000 completed
Ninety-three had type 1 diabetes mellitus
(41 men, 34.7+-15.1 years old and 20.1+9.5 years of diabetes duration; 52
women, 36.7+-12.8 years old and18.9+10.1 years of diabetes duration).
Ninety-nine had type 2 diabetes (42
men, 66.6+-8.6 years old and disease
duration of 17.1+-7.7 years; 57 women,
66.3+-11.0 years old and diabetes
duration of 18.0+-8.6 years).
The Diabetes and Nutrition Study Group of the Spanish Diabetes Association
damage to blood vessels.
doubles the risk of cardiovascular disease.
The main “macrovascular” disease(related
to atherosclerosis of larger arteries).
peripheral vascular disease.
Diabetic retinopathy which affects blood vessel
formation in the retina of the eye.
Diabetic nephropathy, the impact of diabetes on
the kidneys, can lead to scarring changes in the
Diabetic neuropathy, the impact of diabetes on
the nervous system.
Several studies suggest a link between cognitive
deficit and diabetes.
Globally, as of 2010, an estimated 285 million
people had diabetes, with type 2 making up
about 90% of the cases.
Its incidence is increasing rapidly, and by 2030,
this number is estimated to almost double.
Diabetes mellitus occurs throughout the world,
but is more common (especially type 2) in the
more developed countries. The greatest
increase in prevalence is, however, expected to
occur in Asia and Africa, where most patients
will probably be found by 2030.
Prevalence of diabetes worldwide in 2000 (per 1,000 inhabitants) - world average
If diagnosis confirms the condition of
Diabetes mellitus then medication for reversal
of the condition will be given.
A specific life will be advised to the patient
and the diet will be also controlled according
to the requirement.
The constituent of the diet we be modified
according to the condition of the patient.
It is result of autoimmune disease hence no
specific treatment is present.
But researches has shown that transplantation
of beta cells form healthy donor can decrease
the dependence on the Oral insulin.
Humulin R and Novolin R (regular)
Oral insulin was given to the patients who were
facing the shortage of this enzyme in the body
but sensitivity was still intact for its reception.
Replacement cells for
Type I diabetes transplant of new pancreas cells.
In type I DM reformation of beta cells may lead to
permanent cure of the disease.
Inducing the receptors and transporters may also
effect the type 2 DM.
Using stem cells and growing them to produce the
insulin in the IN VIVO system may eliminate the
In pancreatic β cells, the endoplasmic reticulum (ER) is an
important site for insulin biosynthesis and the folding of newly
synthesized proinsulin. Here, we show that IRE1α, an ERresident protein kinase, has a crucial function in insulin
biosynthesis. (Rhodes, 2004;Rhodes et al., 2005)
IRE1α phosphorylation is coupled to insulin biosynthesis in
response to transient exposure to high glucose; inactivation of
IRE1aphosphorylation hinders insulin biosynthesis. IRE1
activation by high glucose does not accompany XBP-1 splicing
and BiP dissociation but upregulates its target genes such as
• Binding of insulin causes
transphosphorylation of tyrosines on the
receptor Phoshotyrosine residues bind
IRS-1 (insulin receptor substrate – adapter
•„ „ Active PKB is released into the cytosol
„ Where it translocates glucose transporter
• Increases glucose uptake
Diabetes is not a single disease but a
cumulative metabolic failure .
So to cure this we have to focus
simultaneously on many factors but
pancreas will be common in all.
Cellular therapies are more promising than
the chemical ones
The number of functionally intact ß cells in the islet
organ is of decisive importance for the development,
course and outcome of diabetes mellitus. Generally
speaking, the total ß-cell mass reflects the balance
between the renewal and loss of these cells. Assuming
that virtually all forms of diabetes mellitus are
characterized by an insufficient extent of beta cell
replication needed to compensate for the loss or
dysfunction of beta cells occurring in diabetes,
elucidation of the regenerating potential in
experimentally induced diabetic animal would be of
interest as alternative therapy for diabetes.
Rhodes, C.J., Shoelson, S., and Halban, P.A. (2005). Insulin
Biosynthesis,Processing, and Chemistry. In Joslin’s Diabetes Mellitus,
C.R. Kahn, G.C.Weir, G.L. King, A.M. Jacobson, A.C. Moses, and R.J.
Smith, eds. (Boston:Joslin Diabetes Center), pp. 65–82
A.M. jamesshapiro, M.B., B.S., Jonathanr.t. lakey, ph.d., Edmonda.
ryan, M.D the new england journal of medicine,islet transplantation in
seven patients with type 1 diabetes mellitus using a glucocorticoid-free
immunosuppressive regimen volume 343 july 27, 2000.
Kathryn L. Lipson, Sonya G. Fonseca, Shinsuke Ishigaki, Linh X.
Nguyen, Elizabeth Foss, Rita Bortell, Aldo A. Rossini and Fumihiko
Urano Regulation of insulin biosynthesis in pancreatic beta cells by an
endoplasmic reticulum-resident protein kinase IRE1 University of
Massachusetts Medical School, Worcester, Massachusetts 01605.
Research and Clinical Practice, Volume 58, Issue 3, December 2002,
Pages 155-165 Makarand V Risbud, Ramesh R Bhonde.
Research and Clinical Practice, Volume 101, Issue 1, July 2013,
American Diabetes Association. (2003a). Evidence-based nutrition
principles and recommendations for the treatment and prevention of
diabetes and related complications (Position Statement). Diabetes
Care, 26 (Suppl. 1), s51 – s61.
The Diabetes and Nutrition Study Group of the Spanish Diabetes
Association (GSEDNu). (2004b). Diabetes Nutrition and
Complications Trial (DNCT): Trends in nutritional pattern between
1993 and 2000 and targets of diabetes treatment in a sample of
Spanish people with diabetes.Diabetes Care, 27, 984 – 987.
Wild S, Roglic G, Green A, Sicree R, King H (2004). "Global
prevalence of diabetes: Estimates for the year 2000 and
projections for 2030". Diabetes Care 27 (5): 1047–
53.doi:10.2337/diacare.27.5.1047. PMID 15111519.
Williams textbook of endocrinology (12th ed.). Philadelphia:
Elsevier/Saunders. pp. 1371–1435. ISBN 978-1-4377-0324-5.