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Journal of Diabetology | Volume 3
May 16-17, 2019 | Prague, Czech Republic
Diabetes and Endocrinology
27
th
International Conference on
J Diabetol, Volume 3
T
raditionally, diabetes Mellitus has been deemed to be
a chronic hyperglycemic disorder secondary to altered
glucose metabolism. Alternatively, hyperglycemia may be one
of several manifestations in subjects with type 1 and type 2
diabetes Mellitus. Almost all tissues require insulin for entry
of glucose, the possible exceptions being red blood cells, renal
medulla as well as central and peripheral nervous systems.
Hyperglycemia in intravascular compartment and other extra
cellularmilieumaybeattributedtoimpairedglucoseentryinto
endothelial cells of the vessel wall and almost all other cells
including hepatocytes, myocytes of all varieties, adipocytes
and individual cells in most other organs respectively due to
absence of insulin in type 1 and both the insulin resistance
as well as the decline in both phases of insulin secretion
in type 2 diabetes. Albeit, the decline in both phases of
insulin secretion are induced by lack of glucose entry into
pancreatic beta cells. Finally, hyperglycemia is perpetuated
by increased hepatic glucose production caused by into
sustained circulating hyperglucagonemia secondary to lack
of glucose entry into the pancreatic alpha cells. Alternatively,
both the decline in insulin secretion by the beta cells and the
rise in glucagon release by the alpha cells are enhanced by
fall in GLP1 and GIP caused by dysfunction of L cells and K
cells respectively secondary to lack of glucose entry in both
type 1 and type 2 diabetes. Similarly, increased prevalence
of infections and thromboembolic micro and macrovascular
events may be attributed to dysfunction of leukocytes and
platelets respectively due to impaired glucose entry. Finally,
alterations in several other metabolemics including serum
concentrations of Adiponectin (Adipose cells), TNF alpha,
Plasminogen inhibitor factor 1, Homocysteine, CRP, Lipids etc.
(Hepatocytes) as well as dysfunction of several organs (liver,
heart, kidney, adrenal, pituitary, lungs etc.) in both type
1 and type 2 diabetes may also be attributed to the lack
of glucose entry into these specific cells. This hypothesis
is validated by improvement in metabolemics and organ
function on facilitation of glucose entry into cells by insulin
administration and/or improvement in insulin sensitivity.
Therefore, in conclusion, diabetes mellitus is a disorder
manifesting dysfunction involving almost all organs and
cells induced by lack of entry of glucose, the most efficient
substrate for cellular function.
Speaker Biography
Udaya M Kabadi is a graduate of Seth G.S. Medical College, the University
of Bombay in Bombay, India. He completed his internal medicine residency
at KEM Hospital Parel in Bombay and a medicine residency at Jewish
Memorial Hospital and Beth Israel Medical Center in New York, He also
completed a fellowship in endocrinology and metabolism at VA Medical
Center and Beth Israel Medical Center in New York. He is board certified in
internal medicine, endocrinology and metabolism and geriatric medicine
by the American Board of Internal Medicine. He is a fellow of the Royal
College of Physicians of Canada, the American College of Physicians and the
American College of Endocrinology. He has been a chief editor, associate
editor and member of editorial boards of several medical journals. He is
currently an adjunct professor of Medicine at the University of Iowa College
of Medicine, Iowa City as well as Des Moines University, Des Moines,
Iowa. He has over 200 publications in peer-reviewed journals. He has
presentations to his credit, at regional, national, and international arenas.
He has been selected as ‘Teacher of the Year’ many times by students,
residents, and fellows in training. He has been involved in research in the
area of carbohydrate metabolism and diabetes, thyroid disorders and
osteoporosis as well as in clinical practice and education for several years.
e:
ukabadi@gmail.comUdaya M Kabadi
1,2
1
Broadlawns Medical Center, USA
2
University of Iowa, USA
Diabetes Mellitus: Disorder of cellular dysfunction due to lack of
entry into cell of glucose; the most efficient fuel for cellular function