Hormones are chemical signals that are released by cells in one part of the body that travel through the bloodstream to signal cells in another part of the body. Insulin is a hormone that is released by the pancreas that induces the uptake of glucose molecules from the bloodstream into cells. In this way, insulin lowers the overall blood glucose levels of the body. Osteoblasts and osteoclasts are two types of bone cells that play a role in regulating blood glucose levels (Figure 1). Binding of insulin to the insulin receptor on osteoblasts activates a signaling pathway that results in osteoblastsreleasing a molecule, OPG, that binds to neighboring osteoclasts. In response, the osteoclasts release protons (H+) and create an area of lower pH outside the cell. This low pH activates osteocalcin, a protein secreted in an inactive form by osteoblasts.The Esp gene encodes a protein that alters the structure of the insulin receptor on osteoblasts and interferes with the binding of insulin to the receptor. A researcher created a group of osteoblasts with an Esp mutation that prevented the production of a functional Esp product (mutant). The researcher then exposed the mutant strain and a normal strain that expresses Esp to glucose and compared the levels of insulin in the blood near the osteoblasts (Figure 2). Based on the information provided, which of the following best justifies the claim that osteocalcin is ahormone? a.The activation of the osteocalcin by a bone cell is pH dependent. b.The osteoblasts in the bone secrete osteocalcin, which causes cells in the pancreas to change their activity. c.The phosphorylation of the insulin receptor causes a response in osteoblast bone cells. d.The change in expression of Esp changes the insulin receptor activity of the osteoblast. ### Blood Insulin Levels in Normal and Mutant Mice After Glucose Injection#### Figure Description:Figure 2 depicts blood insulin levels in normal mice and a specific type of mutant mice referred to as 'Bap' mutant mice over a 60-minute period following glucose injection.#### Graph Details:- **X-axis:** "Minutes After Glucose Injection" ranging from 0 to 60 minutes.- **Y-axis:** "Blood Insulin (ng/mL)" ranging from 0.2 to 1.2 ng/mL.- **Legend:** - Open circles represent data for "Normal" mice. - Filled circles represent data for "Mutant" mice.#### Explanation:- Immediately after glucose injection (0 minutes), both normal and mutant mice have comparable insulin levels (around 0.5 ng/mL).- **For Normal Mice** (open circles; dashed line): - At approximately 5 minutes after injection, there's a sharp spike in insulin levels peaking slightly below 1.0 ng/mL. - This is followed by a decline, stabilizing around 0.4 ng/mL at 10 minutes. - From 10 minutes onwards, the insulin level remains relatively constant, staying under 0.5 ng/mL up to 60 minutes.- **For Mutant Mice** (filled circles; solid line): - There is a gradual increase in insulin levels post-injection. - Starting from around 0.5 ng/mL at 5 minutes, the levels rise steadily over time, reaching approximately 0.8 ng/mL at 60 minutes.#### Interpretation:The data suggests that normal mice exhibit a rapid and transient insulin response to glucose injection, while the mutant mice demonstrate a slower but sustained increase in insulin levels post-glucose injection. This could imply differences in insulin regulation or sensitivity between the two groups, potentially offering insights into the genetic impact on glucose metabolism.#### Conclusion:This figure provides a clear comparative analysis of insulin responses between normal and Bap mutant mice, offering valuable information for understanding genetic influences on metabolic processes. **Figure 1: Pathway Activated by Insulin Binding to the Insulin Receptor**This diagram details the cellular and molecular interactions that occur when insulin binds to an insulin receptor, focusing on the activities within bone cells.**Components and Interactions**:1. **Insulin** acts as a signal that binds to specific receptors.2. **Insulin Receptor**: Embedded in the membrane of osteoblasts (bone-forming cells), this receptor initiates a series of downstream effects when bound by insulin.3. **Osteoblast**: These cells respond to insulin binding by producing Esp Protein and OPG (Osteoprotegerin).**Mechanisms**:- **Esp Protein**: Produced within osteoblasts, though its specific pathway in this diagram isn't detailed.- **OPG (Osteoprotegerin)**: Served as a decoy receptor for RANKL, preventing it from binding to RANK on osteoclast precursors, thus inhibiting their maturation into active osteoclasts.**Osteoclast Activities**:- **In the presence of insulin**: Insulin receptor activation promotes osteoclast activity.- **Osteoclasts**: These cells are responsible for bone resorption. Active osteoclasts secrete hydrogen ions (H+, represented in the diagram) which lower the pH to 4.5 or less, leading to the acidic environment necessary for bone matrix breakdown and activation of inactive osteocalcin into active osteocalcin.**Active Osteocalcin**: Released from bone matrix breakdown, it acts on pancreatic cells influencing insulin secretion.**Pancreas Interaction**:- **Insulin-Secreting Cells of the Pancreas**: These cells have receptors for active osteocalcin. When osteocalcin binds to these receptors, it stimulates further insulin secretion.**Feedback Loop**:- The process forms a feedback loop where insulin influences the activity of bone cells, and bone cell products (such as active osteocalcin) in turn influence insulin secretion from the pancreas.This illustration highlights the complex interactions between insulin signaling, osteoblast and osteoclast activities, and the tight regulation of bone metabolism and endocrine signaling.

Hormones are signaling molecules that help in regulating physiology and behavior. The cells that are…

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Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

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Hormones are chemical signals that are released by cells in one part of the body that travel through the bloodstream to signal cells in another part of the body. Insulin is a hormone that is released by the pancreas that induces the uptake of glucose molecules from the bloodstream into cells. In this way, insulin lowers the overall blood glucose levels of the body. Osteoblasts and osteoclasts are two types of bone cells that play a role in regulating blood glucose levels (Figure 1).

Binding of insulin to the insulin receptor on osteoblasts activates a signaling pathway that results in osteoblasts

releasing a molecule, OPG, that binds to neighboring osteoclasts. In response, the osteoclasts release protons (H+) and create an area of lower pH outside the cell. This low pH activates osteocalcin, a protein secreted in an inactive form by osteoblasts.

The Esp gene encodes a protein that alters the structure of the insulin receptor on osteoblasts and interferes with the binding of insulin to the receptor. A researcher created a group of osteoblasts with an Esp mutation that prevented the production of a functional Esp product (mutant). The researcher then exposed the mutant strain and a normal strain that expresses Esp to glucose and compared the levels of insulin in the blood near the osteoblasts (Figure 2).

Based on the information provided, which of the following best justifies the claim that osteocalcin is a

hormone?

a.The activation of the osteocalcin by a bone cell is pH dependent.

b.The osteoblasts in the bone secrete osteocalcin, which causes cells in the pancreas to change their activity.

c.The phosphorylation of the insulin receptor causes a response in osteoblast bone cells.

d.The change in expression of Esp changes the insulin receptor activity of the osteoblast.

### Blood Insulin Levels in Normal and Mutant Mice After Glucose Injection

#### Figure Description:
Figure 2 depicts blood insulin levels in normal mice and a specific type of mutant mice referred to as 'Bap' mutant mice over a 60-minute period following glucose injection.

#### Graph Details:
- **X-axis:** "Minutes After Glucose Injection" ranging from 0 to 60 minutes.
- **Y-axis:** "Blood Insulin (ng/mL)" ranging from 0.2 to 1.2 ng/mL.
- **Legend:**
- Open circles represent data for "Normal" mice.
- Filled circles represent data for "Mutant" mice.

#### Explanation:
- Immediately after glucose injection (0 minutes), both normal and mutant mice have comparable insulin levels (around 0.5 ng/mL).
- **For Normal Mice** (open circles; dashed line):
- At approximately 5 minutes after injection, there's a sharp spike in insulin levels peaking slightly below 1.0 ng/mL.
- This is followed by a decline, stabilizing around 0.4 ng/mL at 10 minutes.
- From 10 minutes onwards, the insulin level remains relatively constant, staying under 0.5 ng/mL up to 60 minutes.
- **For Mutant Mice** (filled circles; solid line):
- There is a gradual increase in insulin levels post-injection.
- Starting from around 0.5 ng/mL at 5 minutes, the levels rise steadily over time, reaching approximately 0.8 ng/mL at 60 minutes.

#### Interpretation:
The data suggests that normal mice exhibit a rapid and transient insulin response to glucose injection, while the mutant mice demonstrate a slower but sustained increase in insulin levels post-glucose injection. This could imply differences in insulin regulation or sensitivity between the two groups, potentially offering insights into the genetic impact on glucose metabolism.

#### Conclusion:
This figure provides a clear comparative analysis of insulin responses between normal and Bap mutant mice, offering valuable information for understanding genetic influences on metabolic processes.

**Figure 1: Pathway Activated by Insulin Binding to the Insulin Receptor**

This diagram details the cellular and molecular interactions that occur when insulin binds to an insulin receptor, focusing on the activities within bone cells.

**Components and Interactions**:
1. **Insulin** acts as a signal that binds to specific receptors.
2. **Insulin Receptor**: Embedded in the membrane of osteoblasts (bone-forming cells), this receptor initiates a series of downstream effects when bound by insulin.
3. **Osteoblast**: These cells respond to insulin binding by producing Esp Protein and OPG (Osteoprotegerin).

**Mechanisms**:
- **Esp Protein**: Produced within osteoblasts, though its specific pathway in this diagram isn't detailed.
- **OPG (Osteoprotegerin)**: Served as a decoy receptor for RANKL, preventing it from binding to RANK on osteoclast precursors, thus inhibiting their maturation into active osteoclasts.

**Osteoclast Activities**:
- **In the presence of insulin**: Insulin receptor activation promotes osteoclast activity.
- **Osteoclasts**: These cells are responsible for bone resorption. Active osteoclasts secrete hydrogen ions (H+, represented in the diagram) which lower the pH to 4.5 or less, leading to the acidic environment necessary for bone matrix breakdown and activation of inactive osteocalcin into active osteocalcin.

**Active Osteocalcin**: Released from bone matrix breakdown, it acts on pancreatic cells influencing insulin secretion.

**Pancreas Interaction**:
- **Insulin-Secreting Cells of the Pancreas**: These cells have receptors for active osteocalcin. When osteocalcin binds to these receptors, it stimulates further insulin secretion.

**Feedback Loop**:
- The process forms a feedback loop where insulin influences the activity of bone cells, and bone cell products (such as active osteocalcin) in turn influence insulin secretion from the pancreas.

This illustration highlights the complex interactions between insulin signaling, osteoblast and osteoclast activities, and the tight regulation of bone metabolism and endocrine signaling.

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