Answer:
B. Glucagon
Explanation:
Glucagon is a pancreatic hormone, secreted by the alpha cells of islets of Langerhans. Whenever the blood glucose level falls, glucagon is released to increase the blood glucose levels. This function of glucagon is quite opposite to the function of insulin and hence both are antagonistic hormones. Insulin reduces the blood glucose where as glucagon increases the blood glucose.
Glucoagon is large polypeptide of 29 amino acids. Since it helps in increasing the blood glucose homeostatic levels it is called as hyperglycemic hormone. It does so by stimulating certain processes such as:
- Stimulating Glycogenolysis i.e breakdown of glycogen to release more glucose from liver.
- Stimulating Gluconeogenesis i.e. synthesis of glucose from non-carbohydrate sources like proteins.
- Glucagon inhibits the process of glycogenesis i.e. synthesis of glycogen, the storage form of glucose.
<span>Lafora disease is the most severe teenage-onset progressive epilepsy, a unique form of glycogenosis with perikaryal accumulation of an abnormal form of glycogen, and a neurodegenerative disorder exhibiting an unusual generalized organellar disintegration. The disease is caused by mutations of the EPM2A gene, which encodes two isoforms of the laforin protein tyrosine phosphatase, having alternate carboxyl termini, one localized in the cytoplasm (endoplasmic reticulum) and the other in the nucleus. To date, all documented disease mutations, including the knockout mouse model deletion, have been in the segment of the protein common to both isoforms. It is therefore not known whether dysfunction of the cytoplasmic, nuclear, or both isoforms leads to the disease. In the present work, we identify six novel mutations, one of which, c.950insT (Q319fs), is the first mutation specific to the cytoplasmic laforin isoform, implicating this isoform in disease pathogenesis. To confirm this mutation's deleterious effect on laforin, we studied the resultant protein's subcellular localization and function and show a drastic reduction in its phosphatase activity, despite maintenance of its location at the endoplasmic reticulum.
I got my information from </span>https://www.ncbi.nlm.nih.gov/pubmed/14722920
Answer::: Brain structures called the hypothalamus and pituitary gland control the menstrual cycle. The hypothalamus triggers the pituitary gland to make hormones that trigger the ovaries to make oestrogen and progesterone. ... Disorders of the hypothalamus, pituitary gland or ovaries can affect menstruation, causing amenorrhoea
