EXCESS Change detected by β-cells in pancreas Increase in insulin secretion Activates enzymes converting glucose to glycogen Increases rate of glucose uptake Levels return to norm DEFICIENCY Change detected by α-cells in pancreas Increase in glucagon secretion Activates enzymes converting glycogen to glucose Levels return to norm Fluctuating External Conditions Features that influence internal environment have a set level → norm Any changes from the norm is called deviation Negative feedback / caused by deviation from norm / change results in return to norm External environment is changing → experienced by body Homeostatic system even out variations experienced by body Liver can store or release glucose Blood is kept at a constant, ideal state Glucose conc. of 80mg cm-3 Tissue fluid surrounds working cell with constant ideal conditions Optimum glucose for respiration Negative Feedback Tends to Restore Systems to their Original Level Homeostasis is achieved by a negative feedback and involves Change in level of an internal factor (change from norm level) Detected by receptors / impulse send to hypothalamus Activates effectors / stimulates corrective mechanism Level of factor returns to norm Factors in blood and tissue fluid must be kept constant: Temp and pH Change affects rate of enzyme-controlled/biochemical reactions Extreme changes denatures proteins Humans maintain constant core body temp between 36-37.8°C Body temp refers to core body temp → limbs may be cooler than 37°C Water potential / avoids osmotic problems → cellular disruption Conc of ions (Na, K, Ca) Temperature Control Blood flows through receptors in the hypothalamus Deviation causes the autonomic nervous system to initiate an appropriate response DEFICIENCY/DROP IN CORE BODY TEMP BY DECREASING HEAT LOSS/INCREASING HEAT PRODUCTION Receptors in hypothalamus detect increase in core temp/temp of blood Heat conversation centre stimulated VASOCONSTRICTION of arterioles Arterioles leading to capillaries in the skin narrow SHUNT VESSELS DILATE Less blood flows to skin surface / less heat is lost by RADIATION Hair raising / greater insulation / humans have less dense hair, therefore, no effect Shivering / rapid contraction and relaxation of muscles / heat produced by RESPIRATION Adrenaline INCREASES METABOLIC RATE of cells //Mammals in cold climates can increase secretion of thyroxine / hormone increases metabolic rate on a more permanent basis VOLUNTARY CENTRE: put on clothes / seek warmer areas / warm drink EXCESS/RISE IN CORE BODY TEMP BY INCREASING HEAT LOSS/REDUCING HEAT PRODUCTION Receptors in hypothalamus detect increase in core temp/temp of blood Heat loss centre stimulated VASODILATION of arterioles Arterioles leading to capillaries in the skin dilate (expand) SHUNT VESSELS CONSTRICT More blood flows to skin surface (capillaries) / heat loss by RADIATION Heat loss by EVAPORATION of sweat / by using energy High(er) rate of sweating leads to a low(er) skin temp VOLUNTARY CENTRE: remove clothing / seek cooler area / cold drink IMG 7-16-11 The Role of Temperature Receptors in the Skin Hypothalamus detects temp fluctuation inside the body/internal environment Skin receptors detect temp changes in external environment Information is sent by nerves to voluntary centres of the brain Voluntary activities (jogging, moving into a shade) are initiated Changes behaviour of human The Structure and Role of the Skin in Temp Regulation Surface area is very large and in direct contact to external environment Skin is divided into two layers: outer epidermis and inner dermis MALPIGHIAN layer is the boundary between these two layers Cells of this layer divide repeatedly by mitosis Older cells are pushed towards the surface/EPIDERMIS Cytoplasm of old cells becomes full of granules / cells die Cells become converted into scales of keratin (waterproof) DERMIS is thicker than epidermis and contains Nerve endings (temp receptors) Blood vessels held together by connective tissue Beneath dermis is a region which contains some subcutaneous fat Adipose tissue (fat storage tissue) provides vital insulations in humans Hypothermia Body temp falls dangerously below normal Heat energy is lost from body more rapidly than it can be produced Brain is affected first → person becomes clumsy and mentally sluggish As body temp falls, metabolic rate falls as well Makes body temp fall even further, causing a POSITIVE FEEDBACK Temp is taken further away from the norm Death when core body temp is below ≈25°C / by ventricular fibrillation / normal beating of the heart is replaced by uncoordinated tremors Most at risk are (1) babies and (2) elderly (1) High surface area:volume ratio, undeveloped temp regulation mechanisms (2) Detoriated thermoregulatory mechanisms Deliberate hypothermia is sometimes used in surgical operations on heart Patient is cooled by Circulating blood through a cooling machine Placing ice packs in contact with the body Reduces metabolic rate / O2 demand by brain + other vital tissues is lowered Heart can be stopped without any risks of the patient suffering brain damage through lack of O2 Tissues may be permanently damaged if patient is cooled to long Control of Blood Glucose Concentration The Factors which Influence Blood Glucose Concentration Digestion of carbohydrates in diet Digestion → polysaccharide → glucose Fluctuation of glucose blood level depend on amount + type of carbohydrate eaten Breakdown of glycogen Excess glucose → glycogen → glucose Storage polysaccharide made from excess glucose by glycogenesis Glycogen is abundant in liver + muscles Conversion of non-carbohydrates to glucose by gluconeogenesis Oxidation of glucose by respiration Glucose → ATP → energy Rate of respiration varies for different activities This affects glucose uptake from blood into cells Brain is unable to store carbohydrates Lack of glucose in blood → no respiratory substrate → insufficient energy for brain Short period of time already causes brain to malfunction Normal glucose level in blood ≈90mg per 100cm² After a meal it rarely exceeds 150mg per 100cm² The Pancreas Endocrine role is to produce hormones Contains islets of Langerhans → sensitive to blood glucose conc Islet cells contain α-cells → secrete glucagon and β-cells → secrete insulin capillaries into which hormones are secreted delta cells → produce hormone somatostatin → inhibits secretion of glucagon Insulin mainly affects muscles, liver, adipose tissue Exocrine role is to produce digestive enzymes Active trypsin damages pancreas / digests proteins that make up pancreas / amylase leaks into blood from damaged tissues / amylase conc in blood higher High Blood Glucose Concentration Detected by β-cells in islet of Langerhans (receptor) → secrete insulin Increase in insulin secretion (corrective mechanism → effectors bring about a return to norm) Speeds up rate of glucose uptake by cells from blood Glucose enters cells by facilitated diffusion via glucose carrier proteins Cells have vesicles with extra carrier molecules present in their cytoplasm Insulin binds to receptor in plasma membrane Chemical signal → vesicles move towards plasma membrane Vesicle fuses with membrane → increases glucose carrier proteins Activates enzymes / Converts glucose to glycogen / Promotes fat synthesis Low Blood Glucose Concentration Detected by α-cells in islets of Langerhans → secrete glucagon Increase in glucagon secretion Hormone activates enzymes in the liver → convert glycogen to glucose Stimulates formation of glucose form other substances such as amino acids Glucose passes out of cells into blood, raising blood glucose conc until norm is reached Diabetes and its Control with Insulin and Manipulation of Carbohydrate Intake Diabetes mellitus → inability of control of blood glucose level High levels of blood glucose because Pancreas becomes diseased → fails to secrete insulin Target cells lose responsiveness to insulin Kidney is unable to reabsorb back into blood all the glucose filtered into its tubules Glucose secreted into urine Craving for sweet food and persistent thirst DIAGNOSTIC: glucose tolerance test Patient swallows glucose solution Blood glucose level measured at regular intervals Two Types of Diabetes Mellitus Type I → insulin dependant/juvenile-onset Occurs in childhood Autoimmune reaction → immune system attacks and destroys own cells Destroys β-cells in islet of Langerhans → unable to produce insulin TREATMENT: insulin given must match glucose intake and expenditure Overdose causes hypoglycaemia (to much glucose withdrawn from blood) Diabetics need to manage their diet and levels of exercise Need to monitor blood glucose conc Type II → insulin independent/late-onset Occurs late in life, more common than type I Causes by gradual loss in responsiveness of cells to insulin TREATMENT: regulated diet Sugar intake must balance with amount of exercises taken Glycogen levels are lower Little insulin / no glucose to glycogen Insulin receptors no longer functional / less glucose taken up by cells Glycogen is an effective storage molecule Insoluble → no osmotic effect Large → cannot diffuse out of cell Branched → easy to break down / hydrolyse to glucose Compact → large amount of glucose stored in small space Insulin Patches Insulin → peptide chains → digested if swallowed by peptidase → had to be injected Treat skin area with ultrasound → disrupts underlying fat tissues Insulin is not soluble in fat Disrupting tissues allows movement through skin Apply patch containing insulin to that area