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Also some researchers saycan causeextreme neonatal hypoglycemia
I diabetescauseshyperglycemia like
medicationcausinghyperglycemia , hyperuricemia
Protease inhibitorscausehyperglycemia , lipodystrophy
Excess fetal insulin ( hyperinsulinemiamay causeneonatal hypoglycemia
Removal of graft - bearing intestinal segmentsledtorecurrence of hyperglycemia
maternal hyperglycemiacausingneonatal hypoglycemia
Excess fetal glyburide dose hyperinsulinemiamay causeneonatal hypoglycemia
Mutationscauseneonatal hypoglycemia
Diseasescan causeneonatal hypoglycemia
gestational diabetesdoes ... causeneonatal hypoglycemia
by Intense Glucose Management(passive) Caused by Neonatal Hypoglycemia
by diabetes(passive) caused byhyperglycemia ... mellitus
Causes of Hypoglycemia ... various factorscan causeneonatal hypoglycemia
the fetusresultingneonatal hypoglycemia
Causes of Neonatal Hypoglycemia ... various factorscan causeneonatal hypoglycemia
a number of reasons(passive) can be caused byNeonatal hypoglycemia
extracellular hyperglycemiacausesintracellular hyperglycemia in
course of diabetescausesintracellular hyperglycemia
Maternal hyperglycemia during labour , even when produced for a few hours by intravenous fluids in mothers without diabetescan causeneonatal hypoglycemia
These postprandial insulin surgescausepostprandial hypoglycemia
Steroidscan causeworsening of hyperglycemia
a lack of suppression of glucagoncausespostprandial hyperglycemia
glucocorticoidcauseshyperglycemia from gluconeogenesis
Loss of first - phase insulin responsecan causepostprandial hyperglycemia
sudden inhibition of glycogenolysis(passive) is caused byPostprandial hypoglycemia
a decrease in additional insulin secretioncausespostprandial hyperglycemia
beta cell destructionleadsto hyperglycemia with hypoinsulinemia
As a result of either insulin deficiency or the body 's resistance to insulin , the level of glucose in the bloodstream increasescausinghyperglycemia
either abnormal control of insulin secretion in pancreatic cells or the deterioration of the action of insulin in peripheral tissues(passive) caused byhyperglycemia
by either a lack of insulin ( due to autoimmune destruction of islet cells ) or insulin resistance(passive) caused byhyperglycemia
either a lack of insulin due to autoimmune destruction of islet cells or insulin resistance(passive) caused byhyperglycemia
by excessive hepatic glucose production , a deficiency in insulin secretion(passive) caused byhyperglycemia
having too much glucose and/or not enough insulin in the body(passive) is caused byHyperglycemia
the absence of insufficient production of or deficiency of response to insulincauseshyperglycemia
the absence of insufficient production of or deficiency of response to insulinwill causehyperglycemia
by excessive hepatic glucose production and peripheral insulin resistance(passive) caused byhyperglycemia
excessive hepatic glucose production and peripheral insulin resistance(passive) caused byhyperglycemia
patients with diabetes mellitus , the absence or insufficient production of insulincauseshyperglycemia
but it can not be used for sugar metabolism due to insulin resistant cells in liver , fat and musclesalso causeshyperglycemia
dehydrationcausesdehydration
to osmotic diuresis dehydration loss of electrolytesleadsto osmotic diuresis dehydration loss of electrolytes
to hyperglycemia as early as 24h postinjectionleadsto hyperglycemia as early as 24h postinjection
osmotic diuresis and severe dehydrationcausingosmotic diuresis and severe dehydration
osmotic diuresis ... leading to excessive losses of water , sodium and potassiumcausesosmotic diuresis ... leading to excessive losses of water , sodium and potassium
from defects in insulin secretion , insulin action , or both diabetic ketoacidosis ( DKAresultingfrom defects in insulin secretion , insulin action , or both diabetic ketoacidosis ( DKA
a solute diuresis resulting in the manifestations of uncontrolled diabetescausesa solute diuresis resulting in the manifestations of uncontrolled diabetes
from defects in insulin secretion , insulin action , or both impaired fasting glucose or impaired glucoseresultingfrom defects in insulin secretion , insulin action , or both impaired fasting glucose or impaired glucose
lower expression and activity of the two ABC genes(passive) may be caused bylower expression and activity of the two ABC genes
to symptoms or risk of acute hyperglycemic complications ( such as diabetic ketoacidosis and hyperglycemic nonketotic comaleadingto symptoms or risk of acute hyperglycemic complications ( such as diabetic ketoacidosis and hyperglycemic nonketotic coma
from impaired insulin secretion , defects in insulin actionresultingfrom impaired insulin secretion , defects in insulin action
long - term microvascular and macrovascular complications , such as nephropathy , neuropathy , retinopathy , and peripheral vascular diseasemay causelong - term microvascular and macrovascular complications , such as nephropathy , neuropathy , retinopathy , and peripheral vascular disease
to acute metabolic complications , such as diabetic ketoacidosis ( DKAmay leadto acute metabolic complications , such as diabetic ketoacidosis ( DKA
in acute metabolic complications such as : Diabetic Ketoacidosis ( DKAmay resultin acute metabolic complications such as : Diabetic Ketoacidosis ( DKA
in acute metabolic complications such as diabetic ketoacidosis ( DKA ) andmay resultin acute metabolic complications such as diabetic ketoacidosis ( DKA ) and
in acute metabolic complications such as diabetic ketoacidosis ( DKA ) and hyperglycemic hyperosmolar nonketotic syndromemay resultin acute metabolic complications such as diabetic ketoacidosis ( DKA ) and hyperglycemic hyperosmolar nonketotic syndrome
long term microvascular and macrovascular complications , such as nephropathy , neuropathy , retinopathy , and atherosclerosismay causelong term microvascular and macrovascular complications , such as nephropathy , neuropathy , retinopathy , and atherosclerosis
long - term microvascular and macrovascular complications , such as nephropathy , neuropathy , retinopathy and atherosclerosiscan causelong - term microvascular and macrovascular complications , such as nephropathy , neuropathy , retinopathy and atherosclerosis
from defects in insulin secretion and insulin actionresultingfrom defects in insulin secretion and insulin action
from defects in insulin secretion or insulin actionresultingfrom defects in insulin secretion or insulin action
in defects in insulin secretion , insulin action , or bothresultingin defects in insulin secretion , insulin action , or both
from defects in insulin action , insulin secretion or bothresultingfrom defects in insulin action , insulin secretion or both
from defects in insulin secretion , insulin action , or bothResultingfrom defects in insulin secretion , insulin action , or both
from defects in insulin secretion , insulin action or bothresultsfrom defects in insulin secretion , insulin action or both
from defects in insulin secretion , insulin action , or eachresultingfrom defects in insulin secretion , insulin action , or each
from defects in insulin secretion , insulin action , orresultingfrom defects in insulin secretion , insulin action , or
from defects in insulin secretion , insulin action , or both A.resultingfrom defects in insulin secretion , insulin action , or both A.
from defects of insulin action insulin secretion or bothresultingfrom defects of insulin action insulin secretion or both
from defects in insulin secretion , insulin actionresultingfrom defects in insulin secretion , insulin action
from the defects of insulin secretion , insulin action or bothresultingfrom the defects of insulin secretion , insulin action or both
oxidative stress via excessive reactive oxygen species ( ROS ) production in the endothelium , which leads to cellular dysfunction and the development of diabetic vascular diseasescausesoxidative stress via excessive reactive oxygen species ( ROS ) production in the endothelium , which leads to cellular dysfunction and the development of diabetic vascular diseases
from defects in insulin secretion and insulin action or both [ 1resultingfrom defects in insulin secretion and insulin action or both [ 1
from defects in insulin secretion , insulin action or both [ 1resultingfrom defects in insulin secretion , insulin action or both [ 1
from defects of insulin action , insulin secretion or both [ 1resultingfrom defects of insulin action , insulin secretion or both [ 1
from defects in insulin secretion , insulin action or both [ 3resultingfrom defects in insulin secretion , insulin action or both [ 3
from defects in insulin secretion , insulin action or both [ 1resultsfrom defects in insulin secretion , insulin action or both [ 1
from a defect in insulin action or deficiency in insulin secretion or both leading to alterations in carbohydrate , lipid and protein metabolismresultingfrom a defect in insulin action or deficiency in insulin secretion or both leading to alterations in carbohydrate , lipid and protein metabolism
in acute metabolic complications such as : Diabetic Ketoacidosismay resultin acute metabolic complications such as : Diabetic Ketoacidosis
to the production of methylglyoxal that is a highly reactive compound disturbing amongst othersleadsto the production of methylglyoxal that is a highly reactive compound disturbing amongst others
from production in insulin secretion , insulin action , or bothresultingfrom production in insulin secretion , insulin action , or both