Fajr prayer

 

 

 

 

 Narrated Muhammad bin `Amr:

We asked Jabir bin `Abdullah about the prayers of the Prophet . He said, "He used to pray Zuhr prayer at midday, the `Asr when the sun was still hot, and the Maghrib after sunset (at its stated time). The `Isha was offered early if the people gathered, and used to be delayed if their number was less; and the morning prayer was offered when it was still dark

Narrated `Umar:

"The Prophet forbade praying after the Fajr prayer till the sun rises and after the `Asr prayer till the sun sets

Holy Quran said in

[78] Establish regular prayers at the sun's decline till the darkness of the night, and the morning prayer and reading: for the prayer and reading in the morning carry their testimony

•     What the normal level and in which time produced in the early morning [ Glucocorticoids , Adrenocorticotropin  ,Thyrotropin, Thyroid hormones , Testosterone  and, Growth hormone] hormones

•      What the effect of this hormones  on carbohydrate metabolism  and glucose blood level

•   What the effect of Estrogen on Growth hormone which act as insulin antagonist inhibit glucose uptake in female

•      What the effect of insulin and how it secreted to maintain normal glucose blood level

•      Why Fajr prayer we should offer it  before  sun rise

 

Effects of Glucocorticoids

Effects on Metabolism :

 

Glycogen Metabolism

 

It was known in the mid -19^th century that the adrenal glands are essential for life. Their role in the intermediary metabolism was recognized when it was noted that adrenalectomized animals cannot maintain hepatic glycogen stores and that replacement of adrenalectomized animals. Glucocorticoids activate glycogen syntheses and inactive the glycogen – mobilizing enzyme glycogen phosphorylase. The total amount of glycogen syntheses remains unchanged, but it is activated, but it is activated by dephosphorylation. It is not known whether glucocorticosteroids exert their effects on glycogen syntheses by activating a hepatic phosphatase or indirectly by inactivating glycogen phosphorylase, a phosphatase inhibitor.

 

Gluconeogenesis

 

Glucocorticosteroids increase hepatic glucose production in part by increasing substrate availability as the result of stimulating release of glucogenic amino acids from peripheral tissues, such as skeletal muscle. Their effect is most apparent when a psychological replacement dose is administered to adrenalectomized animals. Glucocorticoids also directly activate key hepatic gluconegenic enzymes, such as glucose – G – phosphatase and phosphoenolpyrtivate carbokinase (PEPGK). The increased PEPCK activity results from glucocorticoid – induced activation of PEPCK gene transcription, which is mediated by interaction of the glucocorticoid receptor complex with a specific GRE located in the 5-flanking region of the gene.

   Other gluconeogenic hormones, such as glucagons and epinephrine, are ineffective without the permissive effect of glucocorticoids. Glucocorticoids enhance the sensitivity of lipolysis to catecholamines in target tissues. The glycerol released during lipolysis provides substrate for glucose production, and released fatty acids provide an energy source for the process. Glucocorticoids also enhance the sensitivity of lactate production to catecholamine stimulation in muscle. Increased sensitivity also underlies the permissive effects of glucocorticoids on glucagons action, but the mechanism is unknown.

 

 

Peripheral Glucose Utilization

 

In addition to mobilizing substrate for hepatic gluconcogenesis glucocorticoids inhibit glucose uptake and utilization by peripheral tissues, in part through inhibition of glucose transport into the cells. The numbers of glucose transporters in adipocytes is decreased by glucocorticoids apparently because transporters mRNA levels are decreased.

 

ADRENOCORTICOTROPIN

 

Physiology

 ACTH is produce by corticothrops, which constitute about 15 percent of anterior pituitary cells and are located principally in he central portion of the gland.

 

ACTH controls the release of cortisol from the adrenal cortex.

 

ACTH is released in pulses with an overriding circadian rhythm. With a normal sleeping pattern, ACTH concentration is highest in the early morning (around 4 A.M.) and lowest in the late evening. The normal diurnal rhythm of plasma cortisol occurs in response to these ACTH changes. In primary adrenal insufficiency (Addison’s disease), cortisol concentrations fall, and ACTH concentration rise. This results in hyper pigmentation owing to the melanocyte-stimulating properties of ACTH. Cortisol administration inhibits ACTH release, a phenomenon dependent on both the rate of rise of cortisol and its absolute concentration. Increased plasma cortisol inhibits CRH-induced ACTH release and also may inhibit CRH release. When pharmacologic doses of glucocorticoids are given for prolonged periods, the hypothalamic pituitary – adrenal cortex axis may remain suppressed for months after the drugs are stopped, probably as the results of prolonged hypothalamic CRH suppression

 

Stress, including hypoglycemia, surgery, and psychic distress stimulates ACTH release

Range of Normal Values for Test of Adrenal Function
Test	Normal Value, Range
Plasma cortisol, mmol/L (g/dL 8 AM          4 PM	140 – 690 (5 – 24) 80 – 330 (3 – 12)

 

Carbohydrate Metabolism: Thyroid hormones stimulates almost all aspects of carbohydrate metabolism, including enhancement of insulin – dependent entry of glucose into cells and increased gluconeogenesis and glycogenolysis to generate free glucose. In human subjects have shown that Thyroid hormone excess induces appreciable insulin resistance at a post – binding site in both hepatic and peripheral tissues and that these resistance is accompanied by increased insulin clearance and compensatory increase in insulin secretion.

 

CIRCADIAN AND ULTRA IAN TSH CHANGES

 

A clear circadian variation exists in basal serum TSH levels in animals, and in humans. This variation should be taken into consideration when basal serum TSH levels are measured in the clinical setting. In most human studies, serum TSH levels begins to rise several hours before the onset of sleep, reaching maximal levels between 2300 and 0400 hours and declining gradually thereafter, with the lowest levels occurring at about 1100 hours. The levels very early in the morning are sometimes slightly above the normal range. Although sleep itself undoubtedly modulates TSH secretion, by reducing pulse amplitude but not pulse frequency, the underlying mechanisms are not clear. Furthermore, a seasonal variation in TSH secretion has been described in patients with primary hypothyroidism receiving constant T replacement therapy, some of these patients have higher basal serum TSH levels in the winter than in the summer. This may be a consequence of temperature effects on the peripheral metabolism of thyroid hormones, but such a difference was not found in euthyroid subjects. Although there is some evidence that estrogens can enhance and androgens reduce serum TSH changes has been found.

 The advent of more sensitive assays for human TSH has allowed more in – depth analysis.

 

Testosterone In Your Body

Testosterone can be either free or bound within the body. Bound testosterone is not available for use, as it is bound to other substances throughout the body. Most of a man's testosterone is bound. The remaining testosterone is called free or bioavailable testosterone. Normal levels of testosterone are between 350 - 1000 ng/dl (nanograms per deciliter). Of this, 97 - 98 percent is bound. Most of the binding occurs to a sex hormone-binding globulin (SHBG). The amounts of SHBG within the blood increase with age. The SHBG traps much of the circulating bioavailable testosterone, making it unavailable to exert its effects on the body. It is the bioavailable testosterone that promotes strength in the muscles and maintains or increases muscle mass, libido and sexual performance. It also improves quality of sleep, increases mental and physical energy, and also promotes improvements in mood and the sense of well-being. Testosterone also plays a role in synthesizing proteins. It affects many metabolic activities, such as the production of blood cells in the bone marrow, formation of bone, lipid (fat) and carbohydrate metabolize and growth of the prostate gland.

Like the gynecological hormones, estrogen and progesterone, androgens are not only responsible for reproduction, but are key molecules in a large number of physiological processes.
One main job of androgens is the modulation of biochemical pathways in producing ATP and enhancing lipolysis and glycolysis. The famous Male Ageing Study demonstrated the connection between the androgen and carbohydrate pathways: hypoandrogenemia was associated with a reduced insulin sensitivity and an impaired glucose Transport.
It is also well known that androgen replacement therapy improves body composition and carbohydrate utilization. This was summarized in an excellent review in the New England Journal of Medicine.
One candidate for this carbohydrate metabolism that is depending on androgens is the glut-4-molecule.
Normally, it is localized inside the cytoplasma and, after stimulation by insulin, is incorporated in the cytoplasmatic membrane, thus facilitating the import of glucose.

The gene for glut-4-molecules was described on chromosome 17; and in the promoter area, there is a special steroid response element, similar to the insulin response element which is stimulated by androgens, enhancing the transcription of the gene and facilitating the import of glucose.
Androgens are not only involved in the transcription of the glut-4-molecule, but they also stimulate second messenger molecules such as protein-kinase or insulin response substrata.
Beside the effect of androgens on the metabolism of carbohydrates, there is also a strong physiological connection between androgens and lipid deposition.

INSULIN

This hormone which is the dominant glucose-lowering hormone suppresses endogenous glucose production and stimulates glucose utilization thereby lowering the plasma glucose concentration. Insulin is secreted from the beta cells of the pancreatic islets into the hepatic portal circulation and acts on the liver and peripheral tissues .It inhibits hepatic glycogenolysis and gluconeognesis and in concert with other factors ( including hyperglycemia and hypoglucagonemia ) converts the liver into an organ of net glucose uptake and fuel storage ( glycogen and triglycerides ) .It also stimulates glucose uptake storage and utilization by other tissues such as muscle and fat In the post absorptive state insulin regulates the plasma glucose concentration primarily by restraining hepatic glucose production Higher levels such as those that occur after meals are required to stimulate glucose utilization Conversely decreased insulin secretion causes increased glucose production and decreased glucose utilization by insulin –sensitive tissues and thus tends to raise the plasma glucose concentration  Insulin is therefore both aglucose lowering regulatory and a glucose raising country regulatory hormone The rate of insulin secretion is regulated by a number of factors the most important of which is glucose . A fall in the plasma glucose concentration has an immediate inhibitory effect on insulin secretion thereby limiting a further fall in the plasma glucose level . Insulin is a potent and critical hormone . Either profound insulin deficiency or marked insulin excess can be lethal but its not only the glucoregulatory hormone .

Pulsatile insulin secretion

Insulin is secreted in a pulsatile manner. Recently it has been shown that almost all (~70–100%) of insulin is secreted in discrete insulin secretory bursts occurring approximately every 6 min. Furthermore, it has been revealed that regulation of the rate of insulin secretion is achieved primarily through modulation of the mass of these discrete insulin bursts. Thus meal ingestion increases insulin secretion by enhancing insulin burst mass by ~50% but also increases pulse frequency by ~50%. Interestingly, the hepatic clearance of insulin is also apparently closely related to the pattern of insulin delivery to the liver. It has been known for many years that the pattern of insulin delivery is abnormal in patients with type 2 diabetes. Recently, with new more sensitive insulin assays (ELISA) and validated methods for pulse detection, it has been possible to examine more precisely the abnormalities of pulsatile insulin in patients with type 2 diabetes. These recent studies suggest that the principal defect of insulin secretion is a deficient pulse mass of insulin with no changes in pulse frequency, and that this defect can be overcome by a period of b cell rest.

 

Comment :

In the earIn the early morning befor sun rises at around 4AM and 5AM  depending   to the season

 1-  Glucocorticoids is in the highest level

Important recent observations include: that the metabolism of cortisol in blood vessels by 11-hydroxysteroid dehydrogenase influences vascular tone and blood pressure; that a similar mechanism influences hepatic sensitivity to insulin; that 11-hydroxysteroid dehydrogenase activity is decreased and vascular sensitivity to glucocorticoids is increased in patients with essential hypertension; and that, in cross-sectional studies, both higher blood pressure and insulin resistance are associated with increased glucocorticoid secretion and sensitivity.

 

2- style="FONT-WEIGHT: normal; FONT-SIZE: 7pt; FONT-STYLE: normal; FONT-FAMILY: Times New Roman; FONT-VARIANT: normal">     Thyroid hormones in the highest level both hormones increase hepatic glucose production

3-     Testosterone at the lowest level these cause reduce insulin sensitivity and impaired glucose transport

4-     Growth hormone  which act as an insulin antagonist inhibit glucose uptake

5-     A number of hormones influence GH release most factors that stimulate GH release potent in women than in men at effect mediated by Estrogen well lead to increase insulin resistance

6-     Contribution  of hepatic insulin resistance

In NIDDM patients with moderate fasting hyperglycemia the liver production of glucose is increased by 0.5 mg/kg/min or about  50g/d above normal This modest increase is the consequence of reduced suppression of hepatic glucose production by insulin and by [morning hormones] gluucocorticoids,thyroid ,GH , low testosterone.estrogen] however both factors play a primary role in the pathogenesis of human NIDDM

 

Comment :

1. For these the Fajr prayer came to control these hormones and insulin resistance      
2. 2-Why the recitation of Quran in the early dawn is witnessed.
3. to prevent stress as will as depression which both  hyperglycemia factor 
4. What I believe there are tow main types of  different origins of  type 2  diabetes

The researchers identified a genetic defect linked to insulin resistance -- a condition in which the body resists the effects of insulin and which usually precedes onset of type 2 diabetes The defect is a needle in a genetic haystack: the abnormal substitution of a single DNA particle out of 2,600 in the gene PC-Yet this one genetic defect has the power to interfere with the ability of insulin to regulate the way cells metabolize glucose.

    Which is acquired type due to {puberty,stress,over weight and obesity, less active lifestyle and who doesn't do at least five times daily short-term exercise, depression, pregnancy }

5.    If any one delay Fajr prayer after sun rise  there will be no any benefit because the action of morning hormones in production of glucose without exercise and preventing stress will not control insulin resistance and the result will be either hyperglycemia ,B_cell exhaution or both