Hormonal communication•Exocrine and endocrine glands•endocrine glands – produce

hormones (chemicals that carry information from one part of the body to another)

•endocrine – means “secreting to the inside”

•exocrine glands – means “secreting to the outside”–not hormones–saliva, enzymes, bile, gastric juices, etc.

Control of blood glucose

concentration

The pancreas

• endocrine and exocrine gland• exocrine – pancreatic juices into

duodenum • endocrine – islets of Langerhans

– alpha cells secrete glucagon (stimulates release of glucose)

– beta cells secrete insulin (stimulates uptake of glucose)

We eat food containing carbohydrates

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The carbohydrates are fully digested to glucose which is absorbed

The pancreas detects the change in blood glucose concentration and releases the appropriate hormone

The control of blood glucose• glucose in blood• stored in liver and muscles as glycogen

(large, insoluble polysaccharide)• normal blood glucose level 80-120

mg/ml• increase in blood glucose

– alpha cells stop secreting glucagon– beta cells secrete insulin

insulin affects many cells especially in liver and muscles *** test ?

– increases absorption of glucose from blood into cells

– increase rate use of glucose in respiration

– increase rate of conversion to glycogen

glucagon affects the activity of liver cells

– stimulates break down of glycogen to glucose

– use of fatty acids as fuel for respiration instead of glucose

– production of glucose from fats– release glucose into blood

Insulin and glucagon

Diabetes mellitus

juvenile-onset diabetes – insulin-dependent diabetes• beta cells incapable of secreting sufficient

insulin, or

• person’s own immune system attacks beta cells

non-insulin dependent diabetes

– pancreas secretes insulin– liver and muscle cells do not respond

After meal

– blood glucose rises– kidneys cannot reabsorb all glucose,

it enters urine– water and salts accompany glucose

into urine– person feels hungry and thirsty

uptake of glucose by cells slow

–use fats and proteins for metabolism

–leads to build up of keto-acids, lowers blood pH

–cause dehydration, salt loss–can cause coma

Pharmaceutical insulin– pig or cow insulin– 1980’s genetically engineered bacteria with

human insulin gene– advantages of human engineered bacterial

insulin• more rapid response• shorter duration of response• less chance of immune response• effective in people not tolerant to animal-derived

insulin• acceptable to people opposed to pig/cattle insulin

Manipulating DNA

Genetic engineering: making direct and specific changes in DNA.

• Cutting DNA• Use restriction enzymes

• Separating DNA• Gel electrophoresis

• Pasting DNA together• Forms “recombinant DNA”

• Making copies of DNA• Polymerase chain reaction (PCR)

Restriction Enzymes• Enzymes that cut

DNA at a specific sequence

• Create sticky ends• Discovered in

bacteria– Used as a way

bacteria defend themselves from viruses

Transformation

High Fructose Corn Syrup

Good or Bad?

Dietary sugars stimulate fatty acid synthesis in adults.

Parks EJ, Skokan LE, Timlin MT, Dingfelder CS.

Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, TX 75390-9052, USA. elizabeth.parks@utsouthwestern.edu

Abstract The goal of this study was to determine the magnitude by which acute consumption of fructose in a morning bolus would stimulate lipogenesis (measured by infusion of 13C1-acetate and analysis by GC-MS) immediately and after a subsequent meal. Six healthy subjects [4 men and 2 women; aged (mean +/- SD) 28 +/- 8 y; BMI, 24.3 +/- 2.8 kg/m(2); and serum triacylglycerols (TG), 1.03 +/- 0.32 mmol/L] consumed carbohydrate boluses of sugars (85 g each) in a random and blinded order, followed by a standardized lunch 4 h later. Subjects completed a control test of glucose (100:0) and a mixture of 50:50 glucose:fructose and one of 25:75 (wt:wt). Following the morning boluses, serum glucose and insulin after 100:0 were greater than both other treatments (P < 0.05) and this pattern occurred again after lunch. In the morning, fractional lipogenesis was stimulated when subjects ingested fructose and peaked at 15.9 +/- 5.4% after the 50:50 treatment and at 16.9 +/- 5.2% after the 25:75 treatment, values that were greater than after the 100:0 treatment (7.8 +/- 5.7%; P < 0.02). When fructose was consumed, absolute lipogenesis was 2-fold greater than when it was absent (100:0). Postlunch, serum TG were 11-29% greater than 100:0 and TG-rich lipoprotein-TG concentrations were 76-200% greater after 50:50 and 25:75 were consumed (P < 0.05). The data demonstrate that an early stimulation of lipogenesis after fructose, consumed in a mixture of sugars, augments subsequent postprandial lipemia. The postlunch blood TG elevation was only partially due to carry-over from the morning. Acute intake of fructose stimulates lipogenesis and may create a metabolic milieu that enhances subsequent esterification of fatty acids flowing to the liver to elevate TG synthesis postprandially.