Homeostasis and Behavior pt II

Energy Balance

Not as tightly regulated as water and sodium balance or body temperature

To maintain vital systems functioning

Storing energy helps facilitate survival during times of low energy intake (adipose tissue)

Anticipation can influence hormone production

Meal Anticipation

Smell, Time of Day, Environmental Factors

Increase in GLP-1 an hour before meal

Increase in Ghrelin 2 hours before meal

Increase in insulin 20 mins before meal

Well Fed State

Food is broken down into glucose, free fatty acids, and amino acids, Glucose powers the brain

Insulin is released from the pancreas to facilitate transport of glucose

Excess glucose is converted to glycogen and stored in the liver and muscles (glycogen and lipogenesis)

Cephalic phase facilitates sensory stimuli and stimulates hunger

GI phase storage of excess energy

Fasting State

Glucagon is released from pancreas and glycogenolysis breaks down stored glycogen in the liver (stress can also cause this release)

Lipolysis in adipose tissue releases free fatty acids and glycerol

Liberated glucose and ketone bodies power the brain (brain prefers glucose)

Brain requires constant glucose supply, extended fasting then ketone bodies if no glucose

Muscles can use glucose or fatty acids

Obesity in America

Obesity is on the rise, and most states have an obesity rate of over 30%

Internal Signals that Influence Feeding

Type 2 Diabetes, Heart Disease, Hypercholesterolemia, Stroke, Cancer, Sleep Apnea

Behavioral Endocrinology and Internally Motivated Behaviors

Not completely understood, there is a lot of overlap between the systems

There are two different systems, Orexigenic (feeding) and Anorexigenic (suppressing feeding)

Distinction between hormones in each system is complicated

Insulin Regulation of Metabolism

Secreted from beta cells of pancreas

Two phases, Cephalic and GI

Cephalic: Internal clock, expectation, sensory cues

GI: Food intake

Glucose Storage: Glycogen and Lipogenesis

Epinephrine Regulation of Metabolism

Release of adrenal medulla

Breakdown of glycogen and triglycerides

Glucagon and Regulation of Metabolism

Released from pancreatic alpha cells

Breaks down glycogen

Glucocorticoids and Regulation of Metabolism

Corticosterone/cortisol

Released from adrenal cortex

Breakdown of glycogen

Leptin and Regulation of Food Intake

Peripheral signal

Produced from adipose tissue, circulating levels proportional to body fat

OB/OB mice lack leptin; administration makes them lose weight

Low Leptin during extreme weight loss seems to signal starvation to increase food intake

Body Adiposity

Linked to compensatory changes in food intake

Feeding Stimulatory Circuit: Causes increased food intake and increase energy balance that is stored in adipose tissue. Fat signals can brain to increase feeding, increase energy expenditure and decrease energy balance

Feeding Inhibitory Circuit: Causes a decrease in food intake, increase in energy expenditure and inhibits energy balance

Ghrelin and Regulation of Food Intake

Produced in the GI tract and stimulates food intake

Peaks before mealtime and promotes weight gain

Opposite effect to leptin in hypothalamus and circulating levels inversely correlated to leptin

Dual Center Theory

Lateral Hypothalamus was the hunger center, and Ventromedial Hypothalamus was the satiety center (WRONG)

Lesions to this area damaged dopamine fibers (which decreased their motivation to do anything) not because this was hunger center

VMH lesions disrupted sympathetic control of insulin secretion and affected insulin levels, so all food was converted into fat

How is feeding regulated

Regulated through the hypothalamus and hindbrain, and hormones

Adiposity signals, Nutrients, Social aspects all innervate in hypothalamus (ARC) and through there the pituitary gland signals blood glucose changes, and talks to dorsal and ventral hindbrain

Hindbrain receives inputs from satiety signals and talks to hypothalamus and through the ventral hindbrain monitor blood glucose and food intake

Hypothalamus and Regulating Food Intake

Arcuate Nucleus: Contained two opposing mechanisms for feeding. Stimulatory and Inhibitory inhibit hormones (NPY/AgRP) that produce feeding

Parvoventricular Nucleus (PVN) and Lateral Hypotaltmus: Feeding behaviors

Well Fed State: putting it all together

Increased fat mass causes an increase in leptin and insulin expression and increase their action in the hypothalamus and cause…

Inhibition: NPY/AgRP neurons in the Arcuate Nucleus will be inhibited, decreasing the expression of NPY and AgRP and decrease their release, this leads to a decreased food intake and anorexia

Activation: PONC/CART neurons which increase a-MSH expression and release, combined with signals of low AGRP which inhibit MSH. MSH binding causes activation of melanocortin receptors and decrease food intake

Reduced Food Intake: Putting it all together

Decrease in fat cell mass causes a decrease in leptin/insulin expressing and action in the hypothalamus this causes…

Activation: In NPY/AgRP neurons and an increase in their expression and release. This increases food intake and results in obesity

Inhibition: In POMC/CART neurons and a decrease in a-MSH expression and release, (release of AGRP blocks MSH receptors). MSH expression causes decrease in activity of melanocortin anorexia pathways and an increase in food intake and obesity