India harbours 99 species of scorpions, but not all scorpion stings result in victim death. Only 45 of these species, members of the Buthidae family, can cause fatalities. Elsewhere the most venomous species also belong to the Buthidae family: Androctonus from Algeria, Leiurus quinquestriatus from Israel and Jordan, C entruroides from Mexico, Buthus occitanus from Jordan, Tityus serrulatus from Brazil, Parabuthus from South Africa, Buthus occitanus from Sahara, Tityus trinitatis from Trinidad, and Centruroides sculpturatus from North America and many other countries In spite of zoological differences resulting in venoms of differing chemical structure, the symptomatology following human envenomation is quite similar The effect of the venom depends on the age of the offending scorpion, the season of the year, and the size age and weight of the victim The behavioural changes observed in the experimental animals following envenoming confirmed our earlier reports 19,22 and indicated an autonomic sympathetic and parasympathetic and neuro-muscular over-activity.
The rise in the blood glucose levels observed in this study Tables 1 , 2 could be due to increased glycogenolysis stimulated by increased catecholamines 1,2,,28 , glucagon, cortisol, and changes in insulin secretion. The results of hyperglycaemia due to scorpion envenoming were in accordance with earlier work 16,18,19,24, In this study, both insulin and blood glucose were found to be higher after 60 and after min of venom injection Table 2.
These results confirmed the previous findings 12, Inhibition of insulin release 15 and stimulation of glucagon secretion 14 by toxin from Leiurus quinquestriatus scorpion venom in rat pancreatic islets had already been demonstrated.
These investigations 14,15 have suggested that norepinephrine release from sympathetic nerve endings is probably much greater when stimulated by scorpion venom toxin than by physiologic stimulation. Further, Johnson et al. Glucocorticoids can also be released following stress or injury 8 , as observed in this study.
The sympatho-adrenal axis primarily serves to maintain the pressure flow relationship necessary for organ perfusion. Thus, during the "ebb phase", the insulin levels are reduced and with the onset of hypermetabolism, characteristic of the "flow phase", the hormonal environment is changed 8. The presence of increased circulating levels of any one of these catabolic hormones that is glucagon, glucocorticoids, or catecholamines in a normal individual result in only minimal alterations in the metabolism and circulation 8.
However, in the presence of increased circulating levels of all three catabolic counter-regulatory hormones, the effects of these hormonal actions are synergistic and sustained hepatic glucose production is observed 8. Thus, it appears that the simultaneous elaboration of the counter-regulatory hormones is partly responsible for the pathogenesis of a variety of clinical and biochemical manifestations following scorpion envenoming.
This could be the reason for glycogenolysis in the atria, ventricle, liver, and skeletal muscles 4,5,21,22,24 , hyperglycaemia 21,22,24 , lipolysis and its products 18,22,23,24,27 , increased protein breakdown products under the catabolic influence of the counter-regulatory hormones, and a simultaneous suppressed insulin secretion or insulin resistance.
Hyperinsulinism observed in this study could be equated with insulin resistance. Insulin resistance could be caused by a change in the receptor membrane, a change in hormone-receptor binding characteristics, or a change in post-receptor events 13, Increased secretions of glucagon, cortisol, and catecholamines along with simultaneous reduction in insulin levels or insulin resistance stimulate glycogenolysis in skeletal muscle and promotes lactate production.
Thus, under the conditions existing in scorpion envenoming, lactate is produced but not utilised contributing to lactic acidosis With the disturbed carbohydrate metabolism, dissimilation of fat is incomplete, since 'fats burn in the flame of carbohydrates' leading to ketosis 22 and this is aggravated by low glycogen content in the liver 4,5, Insulin administration reversed the haemodynamic changes and pulmonary oedema in children and adults stung by venomous scorpions 25,31, Insulin administration in adult respiratory distress syndrome ARDS patients with multisystem organ failure MSOF following septic shock resulted in normal biochemical profile, radiological clearance of lungs, and clinical improvement This could be due to insulin favouring glycogen deposition, inhibiting glycogenolysis and promoting glycogenesis, suppressing the mobilisation of fatty acids from adipose tissue, and promoting lipogenesis.
Insulin administration following scorpion envenoming reversed the ECG and metabolic changes in experimental animals 19,21,24 as well as in scorpion sting victims 25,31,32 reducing angiotensin II levels 20 , glycogenesis, and lipogenesis 22, Severe scorpion envenoming is thus a syndrome of fuel-energy deficits and an inability of the vital organs to utilise the existing metabolic substrates.
This ultimately may result in multisystem organ failure MSOF and death. The remaining 55 siblings 32 boys and 23 girls provide control data for this age range. Testing was performed at h after a h fast. The median age was 98 days range, days. Biology Stack Exchange is a question and answer site for biology researchers, academics, and students. It only takes a minute to sign up. Connect and share knowledge within a single location that is structured and easy to search. As I understand, both cortisol and glucagon cause an increase in blood sugar concentrations.
However I don't understand how they work differently or why they work separately. I would be very grateful if someone could explain the seperate roles and functions of these two hormones and also the different effects that they have I believe cortisol also has something to do with promoting lypogenesis in adipose tissue at the trunk of the body and lypolysis at the extremities. Glucagon and cortisol are VERY different types of hormones, though each of them can affect glucose metabolism and effectively can increase glucose concentrations in the blood albeit through different mechanisms.
Glucagon , pictured above, is a 31 amino acid peptide hormone i. Glucagon travels through the blood and acts predominately in the liver on glucagon receptors.
However, sustained glucagon signaling likely has effects on the expression of the enzymes that cause the glucose to be released from the liver as well though that is a discussion for another question. Cortisol , pictured above, is a steroid hormone i. LIPID that is released from the adrenal glands, specifically the zona fasciulata , which is the middle of the three 'layers' of the adrenal gland. Cortisol is referred to as a glucocorticoid and exerts its major effects through changing gene transcription in a variety of cell types.
The way that cortisol does this is by binding its cortisol receptor, which is generally thought to be in the cytoplasm inside the cell. Upon binding of cortisol to the cortisol receptor, that complex is then transported into the nucleus of the cell where it binds DNA and can increase or decrease the transcription or expression of target genes.
In the case of cortisol, these genes are for the enzymes that increase glucose production of the liver, and thus increase the body's capacity to maintain or elevate blood glucose.
There is also some evidence that cortisol has additional effects independent of gene transcription, but that is outside the scope of this question.
As mentioned in the question, both glucagon and cortisol affect glucose metabolism. Epinephrine also promotes the breakdown and release of fat nutrients that travel to the liver and that are converted into sugar and ketones. Cortisol is a steroid hormone also secreted from the adrenal gland. It makes fat and muscle cells resistant to the action of insulin, and enhances the production of glucose by the liver.
Under normal circumstances, cortisol counterbalances the action of insulin. Under stress or if a synthetic cortisol is given as a medication such as with prednisone therapy or cortisone injection , cortisol levels become elevated and you become insulin resistant. When you have Type 2 diabetes, this means your may need to take more medication or insulin to keep your blood sugar under control. Growth Hormone is released from the pituitary, which is a part of the brain.
Like cortisol, growth hormone counterbalances the effect of insulin on muscle and fat cells.
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