Fasting

Holy Quran Says in

 [the Cow  verses]

[185] Ramadan is the (month) in which was sent down the Qur-an, as a guide to mankind, also Clear (Signs) for guidance and judgment (between right and wrong). So every one of you who is present (at his home) during that month should spend it in fasting, but if any one is ill, or on a journey, the prescribed period (should be made up) by days later. Allah intends every facility for you; He does not want to put you to difficulties. (He wants you) to complete the prescribed period, and to glorify Him in that He has guided you; and perchance ye shall be grateful

 

Holy Quran Says  in

 [the Cow  verses ]

[187] and eat and drink until the white thread of dawn appear to you distinct from its black thread; then complete your fast till the night appears; but do not associate with your wives while ye are in retreat in the mosques. Those are limits (set by) Allah: approach not nigh thereto. Thus doth Allah make clear His Signs to men: that they may learn self-restraint.

 

Hadith:

Narrated Abu Huraira:

My friend (the Prophet) advised me to do three things and I shall not leave them till I die, these are: To fast three days every month, to offer the Duha prayer, and to offer witr before sleeping

 

 

Mu'adha said: I asked 'A'isha: What is the reason that a menstruating woman completes the fasts (that she abandons during her monthly course). but she does not complete the prayers? She (Hadrat 'A'isha) said: Are you a Haruriya? I said: I am not a Haruriya, but I simply want to inquire. She said: We passed through this (period of menstruation), and we were ordered to complete the fasts, but were not ordered to complete the prayers.

 

 

Narrated Sahl bin Sa`d:

Allah's Apostle said, "The people will remain on the right path as long as they hasten the breaking of the fast

 

Narrated Sahl bin Sa`d:

I used to take my Suhur meals with my family and then hurry up for presenting myself for the (Fajr) prayer with Allah's Apostle

 

Narrated Anas bin Malik:

The Prophet said, "Take Suhur as there is a blessing in it Hegira Calendar 354-355 day

The muslms should keep fast 30days in ramadan and 43 days ordered how can . these equal 73 days a year 

The prophet forbade the fasting of ‘Id-Ul-Fitr

Glucose metabolism p>

Glucose metabolism

OOrigin and fat of glucose

Glucose is derived from three sources : intestinal absorption that follows digestion of dietary carbohydrates ; glycogenolysis , the breakdown of glycogen which is the polymerized storage from of glucose glycogenolysis the formation of glucose from including  lactate ( and pyuvate ) amino acide ( especially alanine and glutamine ) and to a lesser extent glycerol .

Although most tissues express the enzyme systems re-quired synthesize ( glycogen syntheses ) and hydrolyze ( phose-phorylase ) glycogen , only the liver and kidneys express glucose –6-phosohatase the enzyme  necessary for the release of glucose into the circulation . the liver and kidneys also contain the enzymes necessary for gluconeogenesis .

There are multiple potential metabolic fates for glucose that is transported into sells it maybe stored as glycogen it maybe undergo glycolysis to pyruvate which can be reduced to lactate terminated to form alanine or converted to acetyl coenzyme A which in turn can be oxidized to carbon dioxide and water via the tricarboxylic acid cycle converted to fatty acids ( and stored as triglycerides or utilized for ketone body ( acctocetate B-hydroxy butyrate ) or cholesterol synthesis . Finally glucose maybe released into the circulation .

Hepatic glucose metabolism

The liver is remarkably flexible in its role in glucose homeostasis and is the major source of net endogenous glucose  production under conditions of high glucose  output ( fasting ) the energy needs of the liver are largely provided by the beta oxidation of fatty acids conversely the liver can also be unorgan of net glucose  uptake you be with glucose  stored as glycogen oxidzed for energy or converted to fat which can either remain it liver or be transported to other tissues as very low density lipoproteins  .

 

Counter regulatory hormones

Glucose raising or  Counter regulatory hormones include glucagon epinephrine Growth hormone and cortisol . In response to falling plasma glucose levels glucagon is secreted from the alpha cells of the pancreatic islets into the hepatic portal circulation and is believed to act exclusively on the liver under physiological conditions it activates glycogenolysis and gluconeogenesis and increases hepatic glucose production within minutes .These increases is transient . Despite ongoing hyperglucagoemia glucose  production returns toward basal rates over about 90min although the hormone continues to support glucose production ( I,e., with drawal of glucagon causes a further decrease in glucose production thereafter] Glucagon-  -induced hyperglycemia is also transient because the glucagon –induced increase in glycogenolysis does not persist during sustained hyperglucagonemia  gluconeogenesis increases progressively over at least 4h in dogs  The transient nature of the glycogenolytic response to sustained hypergluccagonemia is not the  result of  glycogen depletion as a further increase in glucose release but it instead the cause a further increase in glucose release but is instead the result of glucose-induced insulin secretion and the autoregula-tory effect of hyperglycemia although other factors may be involved .

 

The hyperglycemic effect of the adrenal hormone epinephrine is more complex The hormone is secreted in response to falling plasma glucose levels and both stimulates hepatic glucose production and limits glucose utilization The actions of epinephrine are both direct and in direct and are mediated through both a- and B-adrenergic receptors a-Adrenergic limitation  of insulin secretion unimportant indirect hyperglycemic action of epinephrine allows the hyperglycemic response to occur although the increase in insulin secretion as plasma glucose rises limits the magnitude of the hyperglycemic response B-adrenergic stimulation of glucagon secretion also occurs but its contribution to the hyperglycemic effect of epinephrine appears to be minor under physiological conditions Epinephrine also acts directly ( independent of changes in other hormones ) to increase hepaticglycogenolysis and gluconeogenesis In humans the hepatic effect is mediated predominantly though ( B2-adrenergic mechanisms although a small direct a-adrenergic stimulation of hepatic glucose broduction has been reported Epinephrine also mobilizes gluconeogenic precursors ( lactate alanine and glycerol )and like glucagon acts within minutes to produce a transient in glucose production and basal rates of glucose production there after In contrast to glucagon however epinephrine also limits glucose utilization by insulin sensitive tissues such as skeletal muscle predominantly through direct B2-adrenrgic mechanisms  because of the persistent effect on glucose utilization sustained hyperepinephrinemia results in persistent hyperglycmia Long term  elevations of Growth hormone and of cortisol limit glucose utilization and stimulate glucose production Initially however .

 Growth hormone has a plasma glucose lowering [insulin like] effect its hyperglycemic effect does not appear for  several hours Similarly cortisol causes an increase in the plasma glucose level after 2 to 3 h The hyperglycemic effect of the combination of glucagon epinephrine and cortisol is greater than the sum effect of each hormone individually these synergistic interactions are potentially relevant to glucose counter regulation .

  Neural glucoregulatory factors

The sympathetic neurotransmitter norepinephrine exerts hyperglycemic actions by mechanisms assumed to be similar to those of epinephrine except that norepinephine is released primarily from terminals  of sympathetic postganglionic neurons These terminals are adjacent to adrenergic receptors on target cells within the innervated tissues  Electrical stimulation of hepatic sympathetic nerves decreases glycogen content increases glucose release and causes hyperglycemia in animals and in humans Parasympathetic stimulation increase hepatic glycogen content and decrease hepatic glucose release It is reasonable to anticipate that peptide neurotransmitters and neuromodulators also affect glucose metabolism .

Substrate glucoregulatory factors

Glucose per se shifts hepatic metabolism in favor of glycogen storage Hepatic glucose autoregulation[namelly the fact that the rate of hepatic glucose production is an inverse function of the plasma glucose concentration independent of hormonal and neural regulatory factors] is an important glucose counter regulatory factor in humans Fatty acids support glucose production and limit glucose oxidation 

They too serve as gluconeogenic precursors. Calculating alanine is also largely derived from glucose (glucose – alanine cycle). Glutamine is a major precursor for new glucose formation, although it too is partially derived from glucose (glucose glutamine cycle). During a fast, muscle can reduce its glucose uptake virtually to zero, oxidize fatty acids for its energy needs and, through proteolysis, mobilize amino acids for transport to the liver to serve as gluconeogenic precursors for net glucose formation.

Although quantitatively less important than muscle, adipose tissue can also use glucose for fatty acids synthesis or formation of glycerol – 3 – phosphate, which can then esterifies fatty acids (derived largely from circulating very – low – density – lipoproteins) to form triglycerides. During a fast, adipocytes decrease their glucose utilization and satisfy energy needs from the beta oxidation of fatty acids. Other tissues, such as the formed elements of the blood and the renal medullae, do not have the capacity to decrease glucose utilization during fasting and therefore produce lactate at relatively fixed rates.

   As mentioned earlier, glucose is the predominant metabolic fuel used by the brain under most conditions. Glucose undergoes terminal oxidation to carbon dioxide and water in the brain. When ketones are plentiful in the circulation, as during prolonged fasting, they can support the majority of the energy needs of the brain and thus reduce its glucose utilization.

 

Systemic Glucose Balance

Maintenance of the normal plasma glucose concentration requires precise matching of glucose utilization and endogenous glucose production or dietary glucose delivery.

Fasting

He post absorptive state is the inter digestive period that begins approximately 5 to 6 h after a meal. However, the term is most commonly used in reference to data obtained after a 10 – to – h overnight fast. In the post absorptive state plasma glucose concentrations are stable; thus glucose production and utilization rates are equal. They average 12 mol/kg/min (1.8 toumol/kg/min (2.2 mg/kg/min) and range from about 10 to 14 u 2.6 mg/kg/min) in normal adults after an overnight fast. Approximately 60% of basal glucose utilization is accounted for by the brain. The remainder is used by glycol zing tissues, such as the formed elements of the blood and the renal medullae and to some extent muscle and fat. Hepatic glucose production results from both glycogenolysis and gluconeogenesis even after an overnight fast. Glycogenolysis may be the predominant source after a typical overnight fast, but gluconeogenesis becomes the predominant source within the first 24 h fasting.

The liver is the predominant source of net endogenous glucose production after an overnight fast. The kidneys, which both use and produce glucose, contribute only about 5%. However, renal and hepatic glucose production is regulated. For example, renal glucose release (largely if not entirely via gluconeogenesis rather than glycogenolysis) accounts for glucose production and virtually all of the increase after 2.5 to 3 h. Thus the common practice of equating endogenous glucose production is not appropriate under some conditions.

The importance of gluconeogenesis in providing new glucose and supporting hepatic glycogen stores after an overnight fast becomes apparent when one considers the limited availability of performed glucose. The glucose pool, namely free glucose in the extra  cellular fluid and in the cells of certain tissues in (primarily in the liver but also small amounts in the kidneys, intestinal mucosa, pancreatic islet cells, brain and blood cells), is about 83 to 111 mmol (15 to 20 g) in the normal adult. Glycogen that can be mobilized to provide circulating glucose (e.g., hepatic glycogen) contains approximately 390 mmol glucose (70g), with a range of about 135 to performed glucose can provide as little as a 3-h supply of glucose and less than an 8 – h supply an average, even at the diminished rate of glucose utilization that occurs during the post absorptive state. Clearly, therefore, gluconeogenesis is important for maintenance of the plasma glucose concentration even during an overnight fast.

If fasting is prolonged to 24 to 48 h the plasma glucose level declines and then stabilizes, hepatic glycogen content falls to less than 55 mmol (10 g), and gluconeogenesis becomes the sole source of glucose production. Because amino acids are the main gluconeogenic precursors that result in net glucose formation, muscle protein is degraded. Glucose utilization by muscle and fat virtually ceases. As lipolysis and ketogenesis accelerate and circulating ketone levels rise, ketones become a major source of fuel for the brain. Thus glucose utilization by the brain declines by about half, resulting in a decrease in the rate of gluconeogenesis required to maintained the plasma glucose concentration and hence in diminished protein wasting. After prolonged fasting (40 d) ketones provide an estimated 80 to 90% of the energy used by the brain, and renal gluconeogenesis provides up to half of the endogenous glucose production.

 

Feeding

After a meal, glucose absorption into the circulation is more than twice the rate of post absorptive endogenous glucose production, depending on the carbohydrate content of the meal and the rate of its digestion and absorption. As glucose is absorbed endogenous glucose production is suppressed and glucose utilization by liver, muscle, and fat accelerates. Thus exogenous glucose is assimilated and the plasma glucose concentration returns to the post absorptive level.

Comment :

1-  Islam order the followers to keep fast during month of Ramadan who an able to fast but who cant like ill or who in journey can delay it to the time when he can

2- IdulFiter comes after Ramadan the prophet forbade the fasting  means only  thirty  days  continual sufficient for B-cell to take long rest

3-  Every month should keep fast  for three days  means B-cell will take short rest

4- The Hegira calendar 354-355 days every year  means Ramadan will come  ten days delay not in fixed time and will cover all  seasons during thirty six years

5-  The fasting starts befor sun rise to sun set but you have to take Suhur [meal befor sun rise] and should hasten the breaking of fasting these equal  to less than  10-12 hours daily

6-  After meal glucose absorption into circulation is more than twice the rate of post absorptive endogenous glucose production and these begins approximately 5-6H after meal Then the liver will cover the rest of the day which equal 7-8H without any effect or disturbance in hepatic glycogen stores

7-  For children  when they become 10 years old  islam order them  to start fasting because the  insulin  resistance begins with sex hormones at that age  in both sex and B-cell has to starts to take rest by fasting

8-  Femal during menstration period should not keep fast because femal hormones in the lowest level but even that B-cell should take rest for thirty days  I mean she has to continue fasting when she is past menstration period what I believe the three days monthly fasting it should be in[13-14-15] from the beginning of  menstration because Estrogen in highest level which is  insulin  resistance factor