Hyperglycaemia Health Dictionary

Diabetes mellitus is a condition characterised by a raised concentration of glucose in the blood due to a de?ciency in the production and/or action of INSULIN, a pancreatic hormone made in special cells called the islet cells of Langerhans.

Insulin-dependent and non-insulindependent diabetes have a varied pathological pattern and are caused by the interaction of several genetic and environmental factors.

Insulin-dependent diabetes mellitus (IDDM) (juvenile-onset diabetes, type 1 diabetes) describes subjects with a severe de?ciency or absence of insulin production. Insulin therapy is essential to prevent KETOSIS – a disturbance of the body’s acid/base balance and an accumulation of ketones in the tissues. The onset is most commonly during childhood, but can occur at any age. Symptoms are acute and weight loss is common.

Non-insulin-dependent diabetes mellitus (NIDDM) (maturity-onset diabetes, type 2 diabetes) may be further sub-divided into obese and non-obese groups. This type usually occurs after the age of 40 years with an insidious onset. Subjects are often overweight and weight loss is uncommon. Ketosis rarely develops. Insulin production is reduced but not absent.

A new hormone has been identi?ed linking obesity to type 2 diabetes. Called resistin – because of its resistance to insulin – it was ?rst found in mice but has since been identi?ed in humans. Researchers in the United States believe that the hormone may, in part, explain how obesity predisposes people to diabetes. Their hypothesis is that a protein in the body’s fat cells triggers insulin resistance around the body. Other research suggests that type 2 diabetes may now be occurring in obese children; this could indicate that children should be eating a more-balanced diet and taking more exercise.

Diabetes associated with other conditions (a) Due to pancreatic disease – for example, chronic pancreatitis (see PANCREAS, DISORDERS OF); (b) secondary to drugs – for example, GLUCOCORTICOIDS (see PANCREAS, DISORDERS OF); (c) excess hormone production

– for example, growth hormone (ACROMEGALY); (d) insulin receptor abnormalities; (e) genetic syndromes (see GENETIC DISORDERS).

Gestational diabetes Diabetes occurring in pregnancy and resolving afterwards.

Aetiology Insulin-dependent diabetes occurs as a result of autoimmune destruction of beta cells within the PANCREAS. Genetic in?uences are important and individuals with certain HLA tissue types (HLA DR3 and HLA DR4) are more at risk; however, the risks associated with the HLA genes are small. If one parent has IDDM, the risk of a child developing IDDM by the age of 25 years is 1·5–2·5 per cent, and the risk of a sibling of an IDDM subject developing diabetes is about 3 per cent.

Non-insulin-dependent diabetes has no HLA association, but the genetic in?uences are much stronger. The risks of developing diabetes vary with di?erent races. Obesity, decreased exercise and ageing increase the risks of disease development. The risk of a sibling of a NIDDM subject developing NIDDM up to the age of 80 years is 30–40 per cent.

Diet Many NIDDM diabetics may be treated with diet alone. For those subjects who are overweight, weight loss is important, although often unsuccessful. A diet high in complex carbohydrate, high in ?bre, low in fat and aiming towards ideal body weight is prescribed. Subjects taking insulin need to eat at regular intervals in relation to their insulin regime and missing meals may result in hypoglycaemia, a lowering of the amount of glucose in the blood, which if untreated can be fatal (see below).

Oral hypoglycaemics are used in the treatment of non-insulin-dependent diabetes in addition to diet, when diet alone fails to control blood-sugar levels. (a) SULPHONYLUREAS act mainly by increasing the production of insulin;

(b) BIGUANIDES, of which only metformin is available, may be used alone or in addition to sulphonylureas. Metformin’s main actions are to lower the production of glucose by the liver and improve its uptake in the peripheral tissues.

Complications The risks of complications increase with duration of disease.

Diabetic hypoglycaemia occurs when amounts of glucose in the blood become low. This may occur in subjects taking sulphonylureas or insulin. Symptoms usually develop when the glucose concentration falls below 2·5 mmol/l. They may, however, occur at higher concentrations in subjects with persistent hyperglycaemia – an excess of glucose – and at lower levels in subjects with persistent hypo-glycaemia. Symptoms include confusion, hunger and sweating, with coma developing if blood-sugar concentrations remain low. Re?ned sugar followed by complex carbohydrate will return the glucose concentration to normal. If the subject is unable to swallow, glucagon may be given intramuscularly or glucose intravenously, followed by oral carbohydrate, once the subject is able to swallow.

Although it has been shown that careful control of the patient’s metabolism prevents late complications in the small blood vessels, the risk of hypoglycaemia is increased and patients need to be well motivated to keep to their dietary and treatment regime. This regime is also very expensive. All risk factors for the patient’s cardiovascular system – not simply controlling hyperglycaemia – may need to be reduced if late complications to the cardiovascular system are to be avoided.

Diabetes is one of the world’s most serious health problems. Recent projections suggest that the disorder will affect nearly 240 million individuals worldwide by 2010 – double its prevalence in 1994. The incidence of insulin-dependent diabetes is rising in young children; they will be liable to develop late complications.

Although there are complications associated with diabetes, many subjects live normal lives and survive to an old age. People with diabetes or their relatives can obtain advice from Diabetes UK (www.diabetes.org.uk).

Increased risks are present of (a) heart disease, (b) peripheral vascular disease, and (c) cerebrovascular disease.

Diabetic eye disease (a) retinopathy, (b) cataract. Regular examination of the fundus enables any abnormalities developing to be detected and treatment given when appropriate to preserve eyesight.

Nephropathy Subjects with diabetes may develop kidney damage which can result in renal failure.

Neuropathy (a) Symmetrical sensory polyneuropathy; damage to the sensory nerves that commonly presents with tingling, numbness of pain in the feet or hands. (b) Asymmetrical motor diabetic neuropathy, presenting as progressive weakness and wasting of the proximal muscles of legs. (c) Mononeuropathy; individual motor or sensory nerves may be affected. (d) Autonomic neuropathy, which affects the autonomic nervous system, has many presentations including IMPOTENCE, diarrhoea or constipation and postural HYPOTENSION.

Skin lesions There are several skin disorders associated with diabetes, including: (a) necrobiosis lipoidica diabeticorum, characterised by one or more yellow atrophic lesions on the legs;

(b) ulcers, which most commonly occur on the feet due to peripheral vascular disease, neuropathy and infection. Foot care is very important.

Diabetic ketoacidosis occurs when there is insu?cient insulin present to prevent KETONE production. This may occur before the diagnosis of IDDM or when insu?cient insulin is being given. The presence of large amounts of ketones in the urine indicates excess ketone production and treatment should be sought immediately. Coma and death may result if the condition is left untreated.

Symptoms Thirst, POLYURIA, GLYCOSURIA, weight loss despite eating, and recurrent infections (e.g. BALANITIS and infections of the VULVA) are the main symptoms.

However, subjects with non-insulindependent diabetes may have the disease for several years without symptoms, and diagnosis is often made incidentally or when presenting with a complication of the disease.

Treatment of diabetes aims to prevent symptoms, restore carbohydrate metabolism to as near normal as possible, and to minimise complications. Concentration of glucose, fructosamine and glycated haemoglobin in the blood are used to give an indication of blood-glucose control.

Insulin-dependent diabetes requires insulin for treatment. Non-insulin-dependent diabetes may be treated with diet, oral HYPOGLYCAEMIC AGENTS or insulin.

Insulin All insulin is injected – mainly by syringe but sometimes by insulin pump – because it is inactivated by gastrointestinal enzymes. There are three main types of insulin preparation: (a) short action (approximately six hours), with rapid onset; (b) intermediate action (approximately 12 hours); (c) long action, with slow onset and lasting for up to 36 hours. Human, porcine and bovine preparations are available. Much of the insulin now used is prepared by genetic engineering techniques from micro-organisms. There are many regimens of insulin treatment involving di?erent combinations of insulin; regimens vary depending on the requirements of the patients, most of whom administer the insulin themselves. Carbohydrate intake, energy expenditure and the presence of infection are important determinants of insulin requirements on a day-to-day basis.

A new treatment for diabetes, pioneered in Canada and entering its preliminary clinical trials in the UK, is the transplantation of islet cells of Langerhans from a healthy person into a patient with the disorder. If the transplantation is successful, the transplanted cells start producing insulin, thus reducing or eliminating the requirement for regular insulin injections. If successful the trials would be a signi?cant advance in the treatment of diabetes.

Scientists in Israel have developed a drug, Dia Pep 277, which stops the body’s immune system from destroying pancratic ? cells as happens in insulin-dependent diabetes. The drug, given by injection, o?ers the possibility of preventing type 1 diabetes in healthy people at genetic risk of developing the disorder, and of checking its progression in affected individuals whose ? cells are already perishing. Trials of the drug are in progress.... diabetes mellitus

A simple sugar that is naturally present in fruits and is a product of the digestion of starch and sucrose. It is the chief source of energy for the body and is carried to all tissues in the blood. The term blood sugar refers to glucose in the bloodstream.The level of glucose in the blood is normally kept fairly constant by the actions of various hormones, notably insulin, glucagon, adrenaline, corticosteroid hormones, and growth hormone. An abnormally high blood glucose level (known as hyperglycaemia) may cause glucose to be lost into the urine. An abnormally low blood glucose level is called hypoglycaemia.... glucose

(Linn.) O. Kuntze.

Family: Ranunculaceae.

Habitat: Western temperate Himalayas from 2,500 to 4,000 m.

English: American cowslip, Marsh Marigold, Water Buttercup.

Folk: Mamiri (Punjab).

Family: Theaceae.

Habitat: Cultivated in Assam, Darjeeling, Travancore, the Nilgiris, Malabar, Bengal, Dehra Dun and Kumaon.

English: Tea.

Unani: Chaai, Shaahi, Shaayi.

Siddha/Tamil: Thaeyilai.

Action: Stimulant, diuretic, astringent. In China, used for diarrhoea and dysentery (causes gastrointestinal upsets and nervous irritability when consumed in excess). Green tea: anticancer effects have been observed in Chinese green tea, Camellia thea, extract; the extract of Japanese green tea showed antihepatotoxic effects.

Important constituents of leaf buds and very young leaves are: caffeine, with a much smaller amount of other xanthines (theophylline and theo- bromine); tannins (the main tannin in green tea is (-)-epigallocatechin); flavonoids, quercetin, kaempferol. The stimulant and diuretic are due to caffeine content, the astringency due to the tannins.

Drinking tea lowers thiamine and thiamine diphosphate losses in urine and blood serum respectively but increases niacin losses. Hot water extract of black tea facilitates Ca absorption in the body experimentally. Tea may decrease zinc bioavailability.

The tea, if added to the meal, significantly lower the availability of iron. Milk is as effective as ascorbic acid in countering the depressing effect of tea on iron availability (in vitro).

The green tea catechin inhibited car- cinogenesis in small intestines when given during or after carcinogen treatment to experimental rats. (-)-epi- gallocatechin gallate and theaflavin di- gallate from green tea inhibited the in- fectivity of both influenza A and B virus (in vitro).

Green tea, when added to a lard- cholesterol diet, decreased the cholesterol and triglyceride levels in fowls. Tea polyphenols exhibit hypocholes- terolaemic activity.

Tea polyphenols—(-)-epicatechin gallate, (-)-epigallocatechine galate, theaflavin monogallate A or B, and or theaflavin digallate—are used for treating hyperglycaemia.

Saponins from tea are used as an- tiulcer agents.

Concurrent use of tea and beta- adrenergic agonists may increase the risk of cardiac arrhythmias. Caffeine, a component of tea, may increase insulin resistance. (Sharon M. Herr.)... camellia sinensis

In severely ill patients – especially those who have had major surgery or those with SEPSIS, burns, acute pancreatitis (see PANCREAS, DISORDERS OF) and renal failure – the body’s reserves of protein become exhausted. This results in weight loss; reduction in muscle mass; a fall in the serum albumin (see ALBUMINS) and LYMPHOCYTE count; and an impairment of cellular IMMUNITY. Severely ill patients are unable to take adequate food by mouth to repair the body protein loss so that enteral or parenteral nutrition is required. Enteral feeding is through the gastrointestinal tract with the aid of a nasogastric tube; parenteral nutrition involves the provision of carbohydrate, fat and proteins by intravenous administration.

The preferred route for the infusion of hyperosmolar solutions is via a central venous catheter (see CATHETERS). If parenteral nutrition is required for more than two weeks, it is advisable to use a long-term type of catheter such as the Broviac, Hickman or extra-corporeal type, which is made of silastic material and is inserted via a long subcutaneous tunnel; this not only helps to ?x the catheter but also minimises the risk of ascending infection.

Dextrose is considered the best source of carbohydrate and may be used as a 20 per cent or 50 per cent solution. AMINO ACIDS should be in the laevo form and should contain the correct proportion of essential (indispensable) and non-essential amino acids. Preparations are available with or without electrolytes and with or without fat emulsions.

The main hazards of intravenous feeding are blood-borne infections made possible by continued direct access to the circulation, and biochemical abnormalities related to the composition of the solutions infused. The continuous use of hypertonic solutions of glucose can cause HYPERGLYCAEMIA and glycosuria and the resultant POLYURIA may lead to dehydration. Treatment with INSULIN is needed when hyper-osmolality occurs, and in addition the water and sodium de?cits will require to be corrected.... parenteral nutrition

Anti-diabetics have an ability to counter hyperglycaemia and are of value for diabetes mellitus.

1st degree. Goat’s Rue, Fenugreek Seeds, Garlic, Jambul.

2nd degree. Damiana, Nettles, Pipsissewa, Olive leaves, Karela, White Horehound, Sweet Sumach, Mountain Grape, Fennel. ... anti-diabetics

See: BREAST MILK.

HYPERGLYCAEMIA. See: DIABETES. To reduce sugar in blood – Guar gum. HYPERHIDROSIS. Excessive sweating. See: PERSPIRATION. ... hypergalactia

The level of glucose in the blood. Abnormally high blood glucose (sometimes called sugar) levels are an indication of diabetes mellitus. (See also hyperglycaemia; hypoglycaemia.)... blood glucose

A state of consciousness between full wakefulness and sleep or unconsciousness. Drowsiness is medically significant if a person fails to awaken after being shaken, pinched, and shouted at, or wakes but relapses into drowsiness.

Abnormal drowsiness may be the result of a head injury, high fever, meningitis, uraemia (excess urea in the blood due to kidney failure), or liver failure.

Alcohol or drugs may also produce this effect.

In a person with diabetes mellitus, drowsiness may be due to hypoglycaemia or to hyperglycaemia.

Abnormal drowsiness should be treated as a medical emergency.... drowsiness

A hormone produced by the pancreas that regulates glucose levels in the blood. It is normally produced in response to raised glucose levels following a meal and promotes glucose absorption into the liver and muscle cells (where it is converted into energy). Insulin thus prevents a build-up of glucose and ensures that tissues have sufficient amounts of glucose. Failure of insulin production results in diabetes mellitus. An insulinoma is a rare tumour that causes excessive production of insulin and consequent attacks of hypoglycaemia.

Insulin replacement, self-administered by injection or through an infusion pump (see pump, insulin), is used in the treatment of diabetes mellitus. Insulin cannot be taken orally because it is destroyed by stomach acid. Preparations are produced from pig or ox pancreas or, more commonly, by genetic engineering. This treatment prevents excessively high glucose levels in blood (hyperglycaemia) and ketosis (a buildup of certain acids in the blood), which, in severe cases, may cause coma.

Too high a dose of insulin will cause hypoglycaemia, which can be relieved by consuming food or a sugary drink.

Severe hypoglycaemia may cause coma, for which emergency treatment with an injection of glucose or glucagon (a hormone that opposes the effects of insulin) is necessary.... insulin

(DKA) a metabolic state resulting from a profound lack of insulin, usually found only in type 1 *diabetes mellitus but sometimes arising in people of Afro-Caribbean ethnicity with type 2 diabetes. Inability to inhibit glucose production from the liver results in *hyperglycaemia, which can be extreme and lead to severe dehydration. The concurrent failure to suppress fatty-acid production from adipose tissue results in the excess conversion of fatty acids to ketones in the liver (*ketosis) and the development of a metabolic *acidosis, which can be severe. Patients often present with vomiting (from the ketosis), which contributes to the dehydration. The condition is treated as a medical emergency with intravenous fluid and insulin; patients should be monitored in high-dependency units.... diabetic ketoacidosis

(glycosylated haemoglobin) any derivative of haemoglobin in which a glucose molecule is attached to the haemoglobin molecule. The most abundant form of glycated haemoglobin is haemoglobin A1c (HbA1c), levels of which are significantly increased in diabetes. The percentage of the HbA molecules that become glycated is dependent on the general level of glucose in the plasma over the lifetime of the molecule (generally three months); this percentage is therefore used as the standard measure of the degree of control of *hyperglycaemia in a person with diabetes over this period. HbA1c values are now expressed in mmol per mol haemoglobin (mmol/mol) rather than as a percentage. The use of HbA1c as a screening tool for diabetes mellitus has become recognized.... glycated haemoglobin

(HHS) a state of extreme hyperglycaemia seen in type 2 diabetes accompanied by dehydration that can be severe, typically triggered by illness in a patient with type 2 diabetes or a patient with previously unknown type 2 diabetes. It was previously known as hyperosmolar non-ketotic hyperglycaemia (HONK). Emergency hospital treatment is required to control blood glucose levels and to treat the dehydration and the underlying precipitating cause. There is a significant mortality, especially in the elderly and patients with other disorders (e.g. vascular disease). While insulin is required as part of the initial emergency treatment, the patient often does not need insulin in the longer term, when well.... hyperosmolar hyperglycaemic state

any one of a class of drugs used in the treatment of HIV infection and *AIDS. Used in combination with other *antiretroviral drugs, they act by inhibiting the action of protease, an enzyme produced by HIV that cleaves two precursor proteins into smaller fragments. These fragments are required for viral growth, infectivity, and replication. Protease inhibitors include atazanavir, indinavir, lopinavir and ritonavir (which are used in combination), saquinavir, and tipranavir. Side-effects include nausea, vomiting, diarrhoea, and rashes; these drugs are also associated with hyperglycaemia and *lipodystrophy. See also boceprevir.... protease inhibitor

These oral agents reduce the excessive amounts of GLUCOSE in the blood (HYPERGLYCAEMIA) in people with type 2 (INSULIN-resistant) diabetes (see DIABETES MELLITUS). Although the various drugs act di?erently, most depend on a supply of endogenous (secreted by the PANCREAS) insulin. Thus they are of no value in treating patients with type 1 diabetes (insulin-dependent diabetes mellitus (IDDM), in which the pancreas produces little or no insulin and the patient’s condition is stabilised using insulin injections). The traditional oral hypoglycaemic drugs have been the sulphonylureas and biguanides; new agents are now available – for example, thiazolidine-diones (insulin-enhancing agents) and alpha-glucosidase inhibitors, which delay the digestion of CARBOHYDRATE and the absorption of glucose. Hypoglycaemic agents should not be prescribed until diabetic patients have been shown not to respond adequately to at least three months’ restriction of energy and carbohydrate intake.

Sulphonylureas The main group of hypoglycaemic agents, these act on the beta cells to stimulate insulin release; consequently they are e?ective only when there is some residual pancreatic beta-cell activity (see INSULIN). They also act on peripheral tissues to increase sensitivity, although this is less important. All sulphonylureas may lead to HYPOGLYCAEMIA four hours or more after food, but this is relatively uncommon, and usually an indication of overdose.

There are several di?erent sulphonylureas; apart from some di?erences in their duration or action (and hence in their suitability for individual patients) there is little di?erence in their e?ectiveness. Only chlorpropamide has appreciably more side-effects – mainly because of its prolonged duration of action and consequent risk of hypoglycaemia. There is also the common and unpleasant chlorpropamide/ alcohol-?ush phenomenon when the patient takes alcohol. Selection of an individual sulphonylurea depends on the patient’s age and renal function, and often just on personal preference. Elderly patients are particularly prone to the risks of hypoglycaemia when long-acting drugs are used. In these patients chlorpropamide, and preferably glibenclamide, should be avoided and replaced by others such as gliclazide or tolbutamide.

These drugs may cause weight gain and are indicated only if poor control persists despite adequate attempts at dieting. They should not be used during breast feeding, and caution is necessary in the elderly and in those with renal or hepatic insu?ciency. They should also be avoided in porphyria (see PORPHYRIAS). During surgery and intercurrent illness (such as myocardial infarction, COMA, infection and trauma), insulin therapy should be temporarily substituted. Insulin is generally used during pregnancy and should be used in the presence of ketoacidosis.

Side-effects Chie?y gastrointestinal disturbances and headache; these are generally mild and infrequent. After drinking alcohol, chlorpropamide may cause facial ?ushing. It also may enhance the action of antidiuretic hormone (see VASOPRESSIN), very rarely causing HYPONATRAEMIA.

Sensitivity reactions are very rare, usually occurring in the ?rst six to eight weeks of therapy. They include transient rashes which rarely progress to erythema multiforme (see under ERYTHEMA) and exfoliate DERMATITIS, fever and jaundice; chlorpropamide may also occasionally result in photosensitivity. Rare blood disorders include THROMBOCYTOPENIA, AGRANULOCYTOSIS and aplastic ANAEMIA.

Biguanides Metformin, the only available member of this group, acts by reducing GLUCONEOGENESIS and by increasing peripheral utilisation of glucose. It can act only if there is some residual insulin activity, hence it is only of value in the treatment of non-insulin dependent (type 2) diabetics. It may be used alone or with a sulphonylurea, and is indicated when strict dieting and sulphonylurea treatment have failed to control the diabetes. It is particularly valuable in overweight patients, in whom it may be used ?rst. Metformin has several advantages: hypoglycaemia is not usually a problem; weight gain is uncommon; and plasma insulin levels are lowered. Gastrointestinal side-effects are initially common and persistent in some patients, especially when high doses are being taken. Lactic acidosis is a rarely seen hazard occurring in patients with renal impairment, in whom metformin should not be used.

Other antidiabetics Acarbose is an inhibitor of intestinal alpha glucosidases (enzymes that process GLUCOSIDES), delaying the digestion of starch and sucrose, and hence the increase in blood glucose concentrations after a meal containing carbohydrate. It has been introduced for the treatment of type 2 patients inadequately controlled by diet or diet with oral hypoglycaemics.

Guar gum, if taken in adequate doses, acts by delaying carbohydrate absorption, and therefore reducing the postprandial blood glucose levels. It is also used to relieve symptoms of the DUMPING SYNDROME.... hypoglycaemic agents

The presence of glucose in the urine.

Glycosuria results from failure of the kidneys to reabsorb glucose back into the bloodstream after the blood has been filtered.

This may be due to hyperglycaemia, as in diabetes mellitus, or may occur if the kidney tubules have been damaged.

However, glycosuria is usually only significant if accompanied by a high blood glucose level.

Glycosuria often occurs during pregnancy when the blood glucose level is normal.

Glycosuria is diagnosed by urinalysis.

Treatment depends on the cause.... glycosuria

combining form denoting a specified biochemical condition of the blood. Example: hyperglycaemia (excess sugar in the blood).... aemia

the concentration of glucose in the blood, normally expressed in millimoles per litre. The normal range is 3.5–5.5 mmol/l. Blood-sugar estimation is an important investigation in a variety of diseases, most notably in diabetes mellitus. See also hyperglycaemia; hypoglycaemia.... blood sugar

type 1 *diabetes mellitus that constantly causes disruption of lifestyle due to recurrent attacks of hypo- or hyperglycaemia from whatever cause. The most common reasons are therapeutic errors, emotional disorders, intercurrent illnesses, and self- or carer-induced episodes.... brittle diabetes

n. a short-acting drug used to control high blood-glucose levels (hyperglycaemia) in patients with type 2 diabetes after diet control has failed (see sulphonylurea). Side-effects are hypoglycaemia, nausea and vomiting, and skin rash.... glipizide

Miers.

Family: Menispermaceae.

Habitat: Himalayas from Simla to Sikkim, Khasi Hills and Assam.

Ayurvedic: Used as Paathaa (Cissampelos pareira).

Folk: Gidaangu (Garhwal), Paahraa (Dehradun).

Action: Tubers—used in pulmonary diseases, asthma, intestinal, disorders and hyperglycaemia.

Alkaloid palmitine exhibits antibiotic activity; stepharine anti-cholines- terase, cycleanine anti-inflammatory and hyndarine sedative activity. Tetra- hydropalmatine produces sedative and anticonvulsant effects on animals (similar but weaker to that of chloropro- mazine). Alkaloids from rhizomes— hypotensive. Pronuciferine hydrochloride—spasmolytic. Root—hypogly- caemic, spasmolytic, CNS active, antimicrobial.... stephania glabra

(Linn.) Skeels.

Synonym: S. jambolanum (Lam.) DC. Eugenia jambolana Lam.

Family: Myrtaceae.

Habitat: Cultivated throughout India up to 1,800 m.

English: Java Plum, Jambolan, Black Plum.

Ayurvedic: Jambu, Mahaaphalaa, Phalendraa, Surabhipatra. (Fruit— black.)

Unani: Jaamun

Siddha/Tamil: Naaval.

Action: Fruit—stomachic, carminative, diuretic. Bark and seed— antidiarrhoeal. Seed—hypo- glycaemic. Leaf—antibacterial, antidysenteric.

Key application: Bark—in nonspecific acute diarrhoea and in topical therapy for mild inflammation of the oral-pharyngeal mucosa; externally in mild, superficial inflammation of the skin. (German Commission E.) The seed has been included among unapproved herbs by German Commission E, as the blood sugar-lowering effect could not be established by several researchers. Claimed applications mentioned in German Commission E monograph: in diabetes, also in combination preparations for atonic and spastic constipation, diseases of the pancreas, gastric and pancreatic complaints.

The Ayurvedic Pharmacopoeia of India recommends the bark in acute diarrhoea and haemorrhagic diseases; the seed in hyperglycaemia and polyuria.

The aqueous alcoholic extract of the bark contains bergenin, gallic acid and ethyl gallate.

The fruit contains anthocyanins and yielded citric, malic and gallic acids. Gallic acid and tannins account for as- tringency of the fruit. Malic acid is the major acid (0.59%) of the weight of fruit; a small quantity of oxalic acid is reported to be present. Glucose and fructose are principal sugars in the ripe fruit; surcose was not detected.

The seeds contain tannin (about 19%), ellagic acid, gallic acid (1-2%), beta-sitosterol, 0.05% essential oil; myricyl alcohol is present in the un- saponifiable matter.

The stem bark yielded friedelan-3- alpha-ol, kaempferol, quercetin, beta- sitosterol and its glycoside, kaempferol- 3-O-glucoside, gallic acid, friedelin and betulinic acid. It contained eugenin and epi-friedelanol. 10-12% tannins were reported.

The leaves contain aliphatic alcohols, sitosterols, betulinic acid and crategolic (maslinic) acid.

The flowers contain triterpenic acids—oleanolic acid and crategolic acid. The oleanolic acid is a strong protector against adriamycin-induced lipid peroxidation in liver and heart microsomes.

Phenols, including methylxantho- xylin and 2, 6-dihydroxy-4-methoxy- acetophene have been isolated from the plant (also from the seed).

Seeds in a dose of 10 mg/kg p.o. on normal and alloxanized rabbits exhibited hypoglycaemic activity up to 23 and 20% respectively. The chloroform fraction of seed extract exhibited potent anti-inflammatory action against both exudative and prolifer- ative and chronic phases of inflammation, besides exhibiting significant anti-arthritic, antipyretic and analgesic activities. Water extract exhibited antibacterial property against S. boydi and S. dysentrae in cases of dysentery and diarrhoea.

The bark extract is reported to have an effect on glycogenolysis and glyco- gen storage in animals.

Dosage: Stem bark—10-20 g for decoction; dried seed—3-6 g powder. (API, Vol. II.)... syzygium cuminii

n. excessive secretion of androgen in women. It is associated with *hirsutism, acne, sparse or infrequent menstruation (oligomenorrhoea), absent or infrequent ovulation, infertility, endometrial *hyperplasia, *hyperlipidaemia, *hyperglycaemia, and hypertension; all these conditions may be the result of mutations in specific genes. See also virilization.... hyperandrogenism

diminution in the response of the body’s tissues to insulin, so that higher concentrations of serum insulin are required to maintain normal circulating glucose levels. Eventually the islet cells can no longer produce adequate amounts of insulin for effective glucose lowering, resulting in hyperglycaemia. Insulin resistance is one of the risk factors for cardiovascular disease. See also diabetes mellitus; metabolic syndrome.... insulin resistance

a condition of postprandial *hypoglycaemia, of varying severity, induced by excessive levels of insulin release from the pancreas. It can be divided into early and late forms, depending on whether the insulin release occurs less than or more than three hours after the meal. The early form is due to the rapid discharge of ingested carbohydrate from the stomach into the small bowel, immediately triggering hyperinsulinaemia. It can occur without obvious cause but is most commonly associated with upper-bowel surgery. The late form is due to a loss of the early-phase insulin response causing excessive postprandial *hyperglycaemia, which then itself triggers an exaggerated insulin response with subsequent hypoglycaemia.... reactive hypoglycaemia