Display Settings:

Format
Items per page

Send to:

Choose Destination
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information

Results: 1 to 20 of 34

1.

Endoplasmic Reticulum Stress

Various physiological or molecular disturbances that impair ENDOPLASMIC RETICULUM function. It triggers many responses, including UNFOLDED PROTEIN RESPONSE, which may lead to APOPTOSIS; and AUTOPHAGY. [from MeSH]

MedGen UID:
465338
Concept ID:
C3178870
Cell or Molecular Dysfunction
2.

Insulin

A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1). [from MeSH]

MedGen UID:
5827
Concept ID:
C0021641
Pharmacologic Substance
3.

Stress

The response of the body to physical, mental, or emotional pressure. This may make a person feel frustrated, angry, or anxious, and may cause unhealthy chemical changes in the body. Untreated, long-term stress may lead to many types of mental and physical health problems. [from NCI]

MedGen UID:
20971
Concept ID:
C0038435
Finding
4.

Unfolded Protein Response

A cellular response to environmental insults that cause disruptions in PROTEIN FOLDING and/or accumulation of defectively folded protein in the ENDOPLASMIC RETICULUM. It consists of a group of regulatory cascades that are triggered as a response to altered levels of calcium and/or the redox state of the endoplasmic reticulum. Persistent activation of the unfolded protein response leads to the induction of APOPTOSIS. [from MeSH]

MedGen UID:
218870
Concept ID:
C1155342
Molecular Function
5.

protein folding

Processes involved in the formation of TERTIARY PROTEIN STRUCTURE. [from MeSH]

MedGen UID:
58195
Concept ID:
C0162847
Molecular Function
6.

insulinoma

A benign tumor of the PANCREATIC BETA CELLS. Insulinoma secretes excess INSULIN resulting in HYPOGLYCEMIA. [from MeSH]

MedGen UID:
43907
Concept ID:
C0021670
Neoplastic Process
7.

Glucose

A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [from MeSH]

MedGen UID:
42238
Concept ID:
C0017725
Pharmacologic Substance
8.

Hyperglycemia

A high level of blood sugar. It is usually an indication of diabetes mellitus. [from NCI]

MedGen UID:
5689
Concept ID:
C0020456
Finding
9.

Dithiothreitol

A reagent commonly used in biochemical studies as a protective agent to prevent the oxidation of SH (thiol) groups and for reducing disulphides to dithiols. [from MeSH]

MedGen UID:
3875
Concept ID:
C0012789
Pharmacologic Substance
10.

Insulinoma

A type of tumor of the pancreatic beta cells that secretes excess insulin and can result in hypoglycemia. [from HPO]

MedGen UID:
506690
Concept ID:
CN167923
Finding
11.

Disease Response

The pathologic and/or clinical changes that result from treatment. The changes may include eradication of detectable disease, stabilization of disease, or disease progression. [from NCI]

MedGen UID:
309976
Concept ID:
C1704632
Finding
12.

Mouse Insulinoma

MedGen UID:
279430
Concept ID:
C1522248
Neoplastic Process
13.

Insulins

Peptide hormones that cause an increase in the absorption of GLUCOSE by cells within organs such as LIVER, MUSCLE and ADIPOSE TISSUE. During normal metabolism insulins are produced by the PANCREATIC BETA CELLS in response to increased GLUCOSE. Natural and chemically-modified forms of insulin are also used in the treatment of GLUCOSE METABOLISM DISORDERS such as DIABETES MELLITUS. [from MeSH]

MedGen UID:
760846
Concept ID:
C3537244
Pharmacologic Substance
14.

Insulin [EPC]

MedGen UID:
453109
Concept ID:
C1579433
Pharmacologic Substance
15.

Postprandial hyperglycemia

Abnormally high BLOOD GLUCOSE level after a meal. [from MeSH]

MedGen UID:
383702
Concept ID:
C1855520
Finding
16.

Disorder of glucose metabolism

Pathological conditions in which the BLOOD GLUCOSE cannot be maintained within the normal range, such as in HYPOGLYCEMIA and HYPERGLYCEMIA. Etiology of these disorders varies. Plasma glucose concentration is critical to survival for it is the predominant fuel for the CENTRAL NERVOUS SYSTEM. [from MeSH]

MedGen UID:
226229
Concept ID:
C1257958
Disease or Syndrome
17.

Antidiabetics

Any substance used to reduce hyperglycemia or treat disorders associated with diabetes. Based on their mechanism of action, this class of agents can be classified to the following groups: directly acting insulomimetics, which activates insulin receptors; indirectly acting insulinomimetics, which increase insulin release such as sulfonylureas or which potentiate the effect of insulin such as metformin; those act directly on the metabolism of glucose such as inhibitors of glucosidases and inhibitors of aldose reductase. [from NCI]

MedGen UID:
183179
Concept ID:
C0935929
Pharmacologic Substance
18.

Murine

MedGen UID:
108834
Concept ID:
C0591833
Pharmacologic Substance
19.

Physiological stress

The unfavorable effect of environmental factors (stressors) on the physiological functions of an organism. Prolonged unresolved physiological stress can affect HOMEOSTASIS of the organism, and may lead to damaging or pathological conditions. [from MeSH]

MedGen UID:
105278
Concept ID:
C0449430
Pathologic Function
20.

Sugar

A white crystalline carbohydrate, typically sucrose, used as a sweetener and preservative. [from NCI]

MedGen UID:
69157
Concept ID:
C0242209
Pharmacologic Substance

Display Settings:

Format
Items per page

Send to:

Choose Destination

Supplemental Content

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...