3. ESSENTIALS
⢠The structure of the walls of the stomach and
small intestine allow them to move, digest, and
absorb food (CORE)
⢠Digestion is controlled by nervous and
hormonal mechanisms. (D2)
⢠The chemical composition of the blood is
regulated by the liver. (D3)
⢠A balanced diet is essential to human health.
(D1)
4. DIGESTION
⢠What is digestion?
⢠Breaking food down into smaller molecules.
⢠This can be done by physically pounding the molecules, or chemically
breaking the molecules apart.
⢠What is the medical term for anything digestive?
⢠GASTRO
⢠What sort of molecules help with chemical digestion?
⢠Enzymes
⢠What kind of gland aids in digestion?
⢠Exocrine â
⢠Produces enzyme
⢠Connected to target organ â DUCT
⢠Glands in DS can be both Exocrine and Endocrine
⢠Which reaction is involved in digestion, hydrolysis or dehydration
synthesis?
⢠Hydrolysis
5. FIVE STAGES OF FOOD
PROCESSING
1. Ingestion
2. Digestion (enzymatic hydrolysis)
3. Absorption â into the blood
4. Assimilation â into the body
5. Egestion
6. MAMMALIAN DIGESTION
⢠Physical digestion â caused by movement
⢠Chemical Digestion â enzymes, water, acids
⢠Accessory glands:
⢠Salivary glands
⢠Pancreas
⢠Liver / Gall bladder
12. ESOPHAGUS
⢠Muscular tubeâŚconnects mouth to stomach.
(epiglottis)
⢠No chemical action. No digestion.
PERISTALSIS â (rhythmic) muscular movement of
food thru the digestive tract after swallowing.
Longitudinal â lengthen
Circular - squeeze
15. STOMACH
The Basics:
⢠J â shaped muscular
organ. Thick walled
⢠Chemical and physical
digestion
⢠Sphincter â cardiac and
pyloric
⢠Stores food
⢠Begins protein
digestionâŚ.
16.
17. STOMACH
⢠Stomach lining:
⢠Contains Gastric Glands:
⢠Has three kinds of cells:
⢠Parietal: Secretes HCl â
activates pepsinogen; denatures
protein; kills pathogen.
⢠Chief: Secretes Pepsinogen;
activates to PEPSIN (gastric
protease) begins protein
digestion. pH â 2.
⢠Neck: Releases mucous;
provides protection
⢠Stomach processes food in 2-
6 hours
⢠Semisolid food: chyme.
18. CONTROL OF GASTRIC JUICE SECRETION
⢠Controlled by nerves and hormones (727-728)
⢠Sight and smell of food sends nerve impulses to Parietal
cells â secretes acid (REFLEX)
⢠Na and Cl ions secreted. Water moves into stomach by
osmosis. Forms Gastric Juice.
⢠Chemoreceptors detect amino acids â move stomach wall.
⢠Impulses are sent to brain. Brain sends impulses to
endocrine glands via VAGUS NERVE to secrete Gastrin.
⢠Gastrin stimulates further secretion of acid and
pepsinogen.
⢠Secretin and Somatostatin - inhibit gastrin secretion
21. SMALL INTESTINE
⢠Small diameterâŚ.7 meters long/ 23 ft (appx)
⢠Some physical; mostly chemical digestion.
⢠Receives secretions from the liver and
pancreas.
⢠3 sections: duodenum (digestion), jejunum
(digestion and absorption) and ileum (for
absorption)
⢠Absorption of nutrients begins in the lining of
the small intestine.
22. SMALL INTESTINE - ENZYMES
⢠Bicarbonate â from pancreas to neutralize acid (not an enzyme)
⢠Protein â
⢠Trypsin - (pancreas) continues protein digestion. (pH 8)
⢠Endopeptidase - (small intestine) completes protein digestion to
amino acids (pH â 7.5)
⢠Fat â
⢠Bile â (liver) not an enzyme. Breaks down large fat molecules
⢠Lipase â (pancreas) digests fats. (pH â 8)
⢠Carbohydrates
⢠Amylase (pancreas) continues starch digestion (disaccharides)
(pH 7)
⢠Maltase - (small intestine) = (maltose into glucose). (pH 7)
⢠Sucrase â glucose and fructose (pH â 7)
⢠Lactase â glucose and galactose (pH â 7)
26. SMALL INTESTINE - FOOD ABSORPTION
⢠Absorbed food travels to the liver for assimilation.
Structure Function
Finger-like shape Large surface area
Surface cell with â microvilli Huge increase in surface area
Surface cells with â enzymes Digestion
Surface cells with â large number of
mitochondria
Active transport and Pinocytosis
Tight Junction Membrane to membrane proteins.
Seals to prevent molecules from passing
between villus
Dense capillary network Blood supply to remove water soluble
nutrients
Lacteal Removes end products of fat digestion.
Lipid soluble vitamins. Part of
lymphatic system
27. METHODS OF ABSORPTION
⢠Simple Diffusion â hydrophobic nutrients â fatty acids
⢠Facilitated Diffusion â hydrophilic nutrients (fructose)
⢠Active Transport â mineral ionsâŚ.Na, Ca, Fe
⢠Endocytosis â Triglycerides, cholesterols
39. ASSIMILATION
⢠Taking molecules to cells to become part of
the body:
⢠Carbohydrates: produce ATP, DNA, RNA,
Cell membrane
⢠Fat: Adipose tissue, phospholipids,
mitochondrial membranes, hormones
⢠Amino acids: cells=proteins. Excessive
amino acids are deaminated by the liver to
form urea
40. LARGE INTESTINE
⢠Larger diameterâŚshorter tube (1.5m)
⢠Sections: cecum, colon (main), rectum
⢠Functions:
⢠Reabsorbs water.
⢠Mutualistic bacteria (E. coli): synthesize
vitamin K
⢠Elimination (egestion) of Waste (Feces)
41.
42. MAIN COMPONENTS OF FECES
⢠CELLULOSE - dietary fiber
⢠LIGNIN - - dietary fiber
⢠BILE PIGMENTS
⢠BACTERIA
⢠INTESTINAL CELLS
⢠MEAN RESIDENCE TIME â
⢠average time undigested âfoodâ remains in the Lg. Intestine.
⢠Positive correlation between the amount of dietary fiber in a personâs diet
the rate of movement through the large intestine.
50. BLOOD FLOW THROUGH THE LIVER
⢠LIVER CELL = HEPATOCYTE
⢠Blood is supplied by these vessels:
⢠HEPATIC PORTAL VEIN â blood from stomach, sm. Int. &
spleen directly to liver. Not a true vein. Bring nutrients to liver.
⢠HEPATIC VEIN â blood -- no Oxygen to heart from liver
⢠HEPATIC ARTERY â blood supplies Oxygen from heart
⢠HPV separates into SINUSOIDS
⢠Capillary- like (wider), thin celled, many pores: allows blood
flowing through it to come in close contact to liver cells.
⢠HA branches to form capillaries that join sinusoids: provides
Oxygen to liver cells.
51.
52. FUNCTIONS
⢠Composed of hepatocytes (Liver cells):
1. Detox: removes toxins from blood. Converts them to less
toxic/non-toxic.
2. Conversion of Cholesterol to Bile Salts: part of BILE. Bile
helps to emulsify fats in small intestine.
3. Production of Plasma proteins: rER of liver cells produce
90% of plasma proteins (Albumin & Fibrinogen). Processed
by Golgi in liver cells
4. Nutrient Storage and Regulation:
⢠GLUCOSE STORAGE â as Glycogen
⢠Storage; Iron, Vitamin A, Vitamin D
⢠Removal of the Amino Group
⢠Conversion of excess Carb & Protein into Fatty Acids
& Triglycerides
⢠Assimilates phospholipids & Cholesterol
55. FUNCTIONS
5. Breakdown of Erythrocytes (RBC)
⢠Kupffer Cells â walls of sinusoids.
⢠Specialized macrophages that absorb and
breakdown RBC by phagocytosis.
⢠Recycle the components:
⢠Hemoglobin split
⢠Globins hydrolyzed
⢠Iron separates from heme â taken to
bone marrow
⢠Remainder of the heme forms BILIRUBIN
â used to form bile.
60. DIET
⢠THE TOTAL FOOD INTAKE BY AN
ORGANISM.
⢠Nutrition â the supply of nutrients.
61. NUTRIENTS
Essential Nutrients â must be consumed as part of your diet. Cannot
be synthesized by the body.
These four nutrients are essential:
⢠Water - essential
⢠Lipids â some types of fatty acid - essential
⢠Amino acids - ½ are essential
⢠Vitamins and Minerals â All minerals & most vitamins
Non-essential â
⢠Carbohydrates â energy can be made from both fats and proteins
62. AMINO ACIDS
⢠20 amino acids
Essential - lacking any a.a not made by the
body
Non essential â any that the body can make
by conversion of other nutrients.
64. FATS
⢠Storage of energy
⢠Insulation of body against temperature changes
⢠Fat around some organs provides shock
absorbers
⢠Cell membrane - phospholipid
65. VITAMIN AND MINERALS
⢠Can be distinguished by their chemical nature
Minerals â
⢠Chemical elements; usually ionic
Vitamins â
⢠All organic
⢠Vitamin K and D â non essential
67. COMPARISON OF ENERGY
IN NUTRIENTS.
⢠Measured in kilojoules (kJ)
CARBOHYDRATES: 1760
kJ/100g
PROTEIN â 1720 kJ/100g
FAT â 4000 kJ/100g
68. MEASURING ENERGY CONTENT
⢠To heat one mL of water 1°celcius â 4.2J of energy is needed
= 1 calorie
⢠SO:
Energy content = temp change(ÂşC) x water volume(mL) x 4.2
of a food mass of food (g)
Calorimeter â instrument used to measure energy content
73. 5. LIPIDS, YOUR HEALTH, AND
HEART DISEASE
Humans can synthesize most fatty acids from carbohydrates
Some Fatty Acids are ESSENTIAL:
⢠Omega 3 â Fatty Acids
⢠Omega 6 â Fatty Acids
Evidence exists linking deficiencies to:
⢠Brain impairments
⢠Maintenance of cardiac tissue
â˘Good sources: Fish, Leafy Vegetables, Walnuts
74.
75. ⢠SATURATED
⢠CHOLESTEROL
⢠TRANS FATS
⢠UNSATURATED
⢠MONOUNSATURATED
⢠POLYUNSATURATED
⢠CIS: OMEGA 3 & 7
GOOD FATS VS. BAD FATS
GOOD BAD
76. CHOLESTEROL LEVEL AS A C.H.D. INDICATOR
HDL vs. LDL â produced in the liver
CHOLESTEROL travels in the blood attached to a protein
⢠Low Density Lipoprotein â transports cholesterol and triglycerides from
the liver around the bodyâŚtends to deposit on artery walls.
⢠âBad cholesterolâ âLousyâ
⢠High Density Lipoproteins - transports excess cholesterol and
triglycerides from body to the liver.
⢠âGood cholesterolâ âHappyâ
Other source of FAT:
⢠Triglycerides - another type of fat produced by excess calories, alcohol,
and sugar (very LDL)
77.
78. CHOLESTEROL AND CORONARY HEART DISEASE
⢠Cholesterol = steroid
Research has shown a positive correlation between high levels of
cholesterol and an increased risk of CHD, but it is not certain that lowering
cholesterol intake reduces the risk of CHD. WHY?
â˘Most research involves total blood cholesterol levels but only
cholesterol in LDL is implicated:
⢠The liver synthesizes its own cholesterol
⢠Saturated and Trans Fat raise cholesterol level
â˘Reducing dietary cholesterolâŚvery little overall effect on CHD
Rates
â˘Genetic factors appear to be more important (less understood)
79. ⢠When youâre HUNGRY:
⢠Stomach releases GHRELIN
⢠Pancreas release GLUCAGON
⢠When youâre FULL (satiety):
⢠Stretch receptors in stomach &
intestine activated
⢠Adipose tissue releases LEPTIN
⢠Sm. Intestine releases CCK
⢠Pancreas releases INSULIN
6. APPETITE CONTROL - HYPOTHALAMUS
Controlled by Hormones Produced:
â˘Pancreas
â˘Stomach
â˘Intestines
â˘FAT (Adipose) Tissue
80. 7. NUTRIENT DEFICIENCY DISEASES/DISORDERS
Malnutrition â a deficiency, imbalance,
or excess of specific nutrients in the
diet.
Starvation â severe lack of intake of both essential and non-
essential nutrients.
⢠Results in breakdown of body tissue
85. VITAMIN D â DEFICIENCY
⢠Calciferol
Needed for calcium absorption in the
intestines.
Symptoms of deficiency similar to calcium
deficiency:
⢠Rickets â soft bone disorder
⢠Bone Fracturing
⢠Muscle atrophy
⢠Dental
⢠Delayed bone growth
⢠Enlargement of liver/spleen
⢠Osteomalacia â bone thinning
⢠Synthesis:
⢠Skin, Food, Supplement
86. PROTEIN MALNUTRITION: PHENYLKETONURIA
PKU CAUSES:
⢠Autosomal recessive â causes a mutation of the
gene for the enzyme PAH
⢠Condition where a baby is unable to breakdown
the a.a. phenylalanine into tyrosine.
⢠Deficiency in the enzyme PAH
⢠Levels of phenylalanine accumulate
88. PHENYLKETONURIA
⢠Most infants are tested soon after birth.
Symptoms:
Early: seizures, small head size
Long term â severe cognitive impairment
Treatment: DIET low in protein
Supplement of essential Amino Acids
91. GENERAL FACTORS THAT CAN
LEAD TO OBESITY (NONMEDICAL)
⢠Food â
⢠high fat and sugar content
⢠Smaller quantities of high fiber
foods eaten
⢠Economic
⢠More unhealthy food is cheaper
⢠Transport
⢠More cars ---- less walking
⢠Jobs
⢠Physically undemanding
⢠Technology
⢠Tasks done by hand
--- now done by
machine.
â˘Video games and
television watching =
âcouch potatoâ
generation!
92. HYPERTENSION
⢠Excess weight:
⢠Places more strain on heart â higher heart rate
⢠Atherosclerosis â narrow blood vessels â higher
heart rate
Precursor to C.H.D.
94. TYPE II - DIABETES
â˘Medical Cause:
⢠Decreased responsiveness of
LIVER, FAT, & MUSCLE
cells to insulin
95. TYPE II - DIABETES
Risk Factors:
⢠Obesity due to overeating
⢠Diets rich in fat/low in fibre
⢠Inactivity
⢠Genetics â parent? Sibling?
⢠Age
⢠Ethnic background
96. TYPE II - DIABETES
Symptoms:
⢠Elevated blood/urine glucose
⢠Frequent Urination
⢠Dehydration/Increased thirst
⢠Extreme hunger
⢠Weight Loss
⢠Fatigue
⢠Slow healing and more frequent infection
97. COMPLICATIONS â TYPE II
DIABETES
If not carefully managed:
⢠Atherosclerosis/circulation issues
⢠Hypertension
⢠CHD
99. ⢠Unusual obsession with food, weight, body shape, and
excessive exercise
⢠Self-imposed starvation
⢠Affects more women than men (as reported)
Psychiatric Condition based on :
⢠Emotional issues
⢠Perfectionism
⢠Control
⢠Self worth
100. PHYSICAL CONSEQUENCES
⢠Circulatory
⢠Anemia - bruising
⢠Low blood cell count & electrolyte balance
⢠Heart failure
⢠Respiratory â lung tissue
⢠Skeletal â bone loss; osteoporosis
⢠Muscle â loss of muscle mass, weaker
⢠Hair Loss
⢠Women â interruption of ovulation
⢠Men â low testosterone
103. JAUNDICE (D3)
⢠Condition in which the skin and eyes become
yellow
⢠Due to accumulation of BILIRUBIN in blood
plasma
⢠Causes: Liver (Hepatitis or Cancer), Gall
Bladder (gall stones), Bile duct disease
⢠Result: could damage the brain, in infants â
cerebralpalsy
104. CHOLERA (D2)
⢠Infection of the intestines
⢠Source: Vibria cholerae (bacteria)
⢠Bacteria releases a toxin that binds to receptors in
the intestines.
⢠Toxin enters cells: endocytosis
⢠Toxin triggers release of Cl & HCO3 Water follows
leading to acute diarrhea.
⢠Fluid loss can cause death within hours
if untreated.
105. STOMACH ACID SECRETION AND ULCERS(D2)
Stomach Acid
â˘secreted by parietal cells
â˘Disrupts ability of cells to be held
together in tissue
â˘Leads to denaturing of proteins
(except pepsin)
106. ACID REFLUX (D2)
⢠occurs when cardiac sphincter malfunctions
⢠Acid enters the esophagus
⢠Production of acid in stomach â
⢠Proton Pump: H+/K+ ATPase
⢠Uses ATP to exchange 2H+ for 2K+ with H+ secreted.
⢠Reduce Acid â
⢠Use of proton pump inhibitor (PPI)
⢠Bind to a single pump â irreversibly â blocks activity â raises
stomach pH
⢠Provides temporary relief
⢠PRILOSEC, PREVACID
107.
108.
109. ULCERS (D2)
⢠Open sore
⢠Partial digestion of stomach lining by pepsin/HCL
⢠Possible Causes:
⢠Infection with Heliobacter pylori bacteria (80%)
⢠Overuse of OTC pain medicine:
NSAID/Aspirin/Ibuprofen
⢠Lack of treatment can lead to stomach cancer
Editor's Notes
PYY3-36
Peptide YY3-36 contains 34 amino acids, many of them in the same positions as those in neuropeptide Y.
But the action of PYY3-36 is just the reverse of that of NPY, being a potent feeding inhibitor. It is released by cells in the intestine after meals. The amount secreted increases with the number of calories ingested and especially when these are derived from proteins rather than carbohydrates or fats. (This may explain the efficacy of the protein-rich, carbohydrate-poor Atkins diet.)
PYY3-36 acts on
the hypothalamus to suppress appetite;
the pancreas to increase its exocrine secretion of digestive juices;
the gall bladder to stimulate the release of bile.
The appetite suppression mediated by PYY3-36 works more slowly than that of cholecystokinin and more rapidly than that of leptin. In a recent human study, volunteers given PYY3-36 were less hungry and ate less food over the next 12 hours than those who received saline (neither group knew what they were getting
istology, adipose tissue or fat is loose connective tissue composed of adipocytes. Adipose tissue is derived from lipoblasts. Its main role is to store energy in the form of fat, although it also cushions and insulates the body. Obesity or being overweight in humans and most animals does not depend on body weight but on the amount of body fatâspecifically, adipose tissue. Two types of adipose tissue exist: white adipose tissue (WAT) and brown adipose tissue (BAT). Adipose tissue also serves as an important endocrine organ[1] by producing hormones such as leptin, resistin and the cytokine TNFÎą. The formation of adipose tissue appears to be controlled by the adipose gene
Leptin binds to the ventromedial nucleus of the hypothalamus, known as the "appetite center." Leptin signals to the brain that the body has had enough to eat, or satiety. A very small group of humans possess homozygous (same on both of the pair) mutations for the leptin gene which leads to a constant desire for food, resulting in severe obesity. This condition can be treated successfully by the administration of recombinant human leptin.[12]
Thus, circulating leptin levels give the brain input regarding energy storage so it can regulate appetite and metabolism. Leptin works by inhibiting the activity of neurons that contain neuropeptide Y (NPY) and agouti-related peptide (AgRP), and by increasing the activity of neurons expressing Îą-melanocyte-stimulating hormone (Îą-MSH). The NPY neurons are a key element in the regulation of appetite; small doses of NPY injected into the brains of experimental animals stimulates feeding, while selective destruction of the NPY neurons in mice causes them to become anorexic. Conversely, Îą-MSH is an important mediator of satiety, and differences in the gene for the receptor at which Îą-MSH acts in the brain are linked to obesity in humans.
PKU" redirects here. For other uses, see PKU (disambiguation).
Phenylketonuria (PKU) is an autosomal recessive genetic disorder characterized by a deficiency in the enzyme phenylalanine hydroxylase (PAH). This enzyme is necessary to metabolize the amino acid phenylalanine to the amino acid tyrosine. When PAH is deficient, phenylalanine accumulates and is converted into phenylpyruvate (also known as phenylketone), which is detected in the urine. PKU is found on chromosome number 12. Phenyl alanine is an ĂÂą-amino acid with the formula HO2CCH(NH2)CH2C6H5. ... The International Statistical Classification of Diseases and Related Health Problems (most commonly known by the abbreviation ICD) provides codes to classify diseases and a wide variety of signs, symptoms, abnormal findings, complaints, social circumstances and external causes of injury or disease. ... The International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) is a coding of diseases and signs, symptoms, abnormal findings, complaints, social circumstances and external causes of injury or diseases, as classified by the World Health Organization (WHO). ... // E00-E35 - Endocrine diseases (E00-E07) Disorders of thyroid gland (E00) Congenital iodine-deficiency syndrome (E01) Iodine-deficiency-related thyroid disorders and allied conditions (E02) Subclinical iodine-deficiency hypothyroidism (E03) Other hypothyroidism (E030) Congenital hypothyroidism with diffuse goitre (E031) Congenital hypothyroidism without goitre (E032) Hypothyroidism due to medicaments and other... The International Statistical Classification of Diseases and Related Health Problems (most commonly known by the abbreviation ICD) provides codes to classify diseases and a wide variety of signs, symptoms, abnormal findings, complaints, social circumstances and external causes of injury or disease. ... The following is a list of codes for International Statistical Classification of Diseases and Related Health Problems. ... The Mendelian Inheritance in Man project is a database that catalogues all the known diseases with a genetic component, and - when possible - links them to the relevant genes in the human genome. ... The Disease Bold textDatabase is a free website that provides information about the relationships between medical conditions, symptoms, and medications. ... Medical Subject Headings (MeSH) is a huge controlled vocabulary (or metadata system) for the purpose of indexing journal articles and books in the life sciences. ... In genetics, the term recessive gene refers to an allele that causes a phenotype (visible or detectable characteristic) that is only seen in a homozygous genotype (an organism that has two copies of the same allele). ... A genetic disorder is a condition caused by abnormalities in genes or chromosomes. ... Categories: Biochemistry stubs | EC 1. ... This article is about the urine of animals generally. ...
Left untreated, this condition can cause problems with brain development, leading to progressive mental retardation and seizures. However, PKU is one of the few genetic diseases that can be controlled by diet. A diet low in phenylalanine and high in tyrosine can be a very effective treatment. There is no cure. Damage done is irreversible so early detection is crucial.
To understand type 2 diabetes, first you must understand how glucose is normally processed in the body.
Glucose is a main source of energy for the cells that make up your muscles and other tissues. Glucose comes from two major sources: the food you eat and your liver. During digestion, sugar is absorbed into the bloodstream. Normally, sugar then enters cells with the help of insulin.
The hormone insulin comes from the pancreas, a gland located just behind the stomach. When you eat, your pancreas secretes insulin into your bloodstream. As insulin circulates, it acts like a key by unlocking microscopic doors that allow sugar to enter your cells. Insulin lowers the amount of sugar in your bloodstream. As your blood sugar level drops, so does the secretion of insulin from your pancreas.
Your liver acts as a glucose storage and manufacturing center. When your insulin levels are low â when you haven't eaten in a while, for example â your liver releases the stored glucose to keep your glucose level within a normal range.
In type 2 diabetes, this process works improperly. Instead of moving into your cells, sugar builds up in your bloodstream. This occurs when your pancreas doesn't make enough insulin or your cells become resistant to the action of insulin. Exactly why this happens is uncertain, although excess fat â especially abdominal fat â and inactivity seem to be important factors.
To understand type 2 diabetes, first you must understand how glucose is normally processed in the body.
Glucose is a main source of energy for the cells that make up your muscles and other tissues. Glucose comes from two major sources: the food you eat and your liver. During digestion, sugar is absorbed into the bloodstream. Normally, sugar then enters cells with the help of insulin.
The hormone insulin comes from the pancreas, a gland located just behind the stomach. When you eat, your pancreas secretes insulin into your bloodstream. As insulin circulates, it acts like a key by unlocking microscopic doors that allow sugar to enter your cells. Insulin lowers the amount of sugar in your bloodstream. As your blood sugar level drops, so does the secretion of insulin from your pancreas.
Your liver acts as a glucose storage and manufacturing center. When your insulin levels are low â when you haven't eaten in a while, for example â your liver releases the stored glucose to keep your glucose level within a normal range.
In type 2 diabetes, this process works improperly. Instead of moving into your cells, sugar builds up in your bloodstream. This occurs when your pancreas doesn't make enough insulin or your cells become resistant to the action of insulin. Exactly why this happens is uncertain, although excess fat â especially abdominal fat â and inactivity seem to be important factors.
Risk factors
Researchers don't fully understand why some people develop type 2 diabetes and others don't. It's clear that certain factors increase the risk, however, including:
Weight. Being overweight is a primary risk factor for type 2 diabetes. The more fatty tissue you have, the more resistant your cells become to insulin.
Inactivity. The less active you are, the greater your risk of type 2 diabetes. Physical activity helps you control your weight, uses up glucose as energy and makes your cells more sensitive to insulin.
Family history. The risk of type 2 diabetes increases if a parent or sibling has type 2 diabetes.
Race. Although it's unclear why, people of certain races â including blacks, Hispanics, American Indians and Asian Americans â are more likely to develop type 2 diabetes.
Age. The risk of type 2 diabetes increases as you get older, especially after age 45. Often, that's because people tend to exercise less, lose muscle mass and gain weight as they age. But type 2 diabetes is increasing dramatically among children, adolescents and younger adults.
Prediabetes. Prediabetes is a condition in which your blood sugar level is higher than normal, but not high enough to be classified as type 2 diabetes. Left untreated, prediabetes often progresses to type 2 diabetes.
Gestational diabetes. If you developed gestational diabetes when you were pregnant, your risk of developing type 2 diabetes later increases. If you gave birth to a baby weighing more than 9 pounds, you're also at risk of type 2 diabetes.
Symptoms
Type 2 diabetes symptoms may seem harmless at first. In fact, you can have type 2 diabetes for years and not even know it. Look for:
Increased thirst and frequent urination. As excess sugar builds up in your bloodstream, fluid is pulled from your tissues. This may leave you thirsty. As a result, you may drink â and urinate â more than usual.
Extreme hunger. Without enough insulin to move sugar into your cells, your muscles and organs become depleted of energy. This triggers intense hunger that may persist even after you eat.
Weight loss. Despite eating more than usual to relieve your constant hunger, you may lose weight. Without the energy sugar supplies, your muscle tissues and fat stores may simply shrink.
Fatigue. If your cells are deprived of sugar, you may become tired and irritable.
Blurred vision. If your blood sugar level is too high, fluid may be pulled from your tissues â including the lenses of your eyes. This may affect your ability to focus.
Slow-healing sores or frequent infections. Type 2 diabetes affects your ability to heal and fight infections. Bladder and vaginal infections can be a particular problem for women.
Some people who have type 2 diabetes have patches of dark, velvety skin in the folds and creases of their bodies â usually in the armpits and neck. This condition, called acanthosis nigricans, is a sign of insulin resistance