Insulin, a hormone produced by the pancreas, plays a central role in regulating how the body uses energy from food. When you eat, carbohydrates are broken down into glucose, which enters the bloodstream. Insulin then acts as a signal, instructing cells to absorb this glucose for immediate energy or to store it for later use.
Insulin resistance develops when the body’s cells, particularly those in muscles, fat, and the liver, do not respond effectively to insulin’s signals. This means glucose has difficulty entering the cells, leading to higher levels of sugar in the blood. The pancreas initially tries to compensate by producing even more insulin, attempting to overcome this cellular unresponsiveness.
The Normal Function of Insulin
In a healthy individual, the pancreas secretes insulin in response to elevated blood glucose levels after consuming food, allowing glucose to enter cells like muscle, fat, and liver cells. Once inside, glucose can be used as fuel for cellular activities.
Insulin also plays a significant role in energy storage. When there is excess glucose in the bloodstream, insulin signals the liver to convert this glucose into glycogen, a stored form of glucose. This glycogen can then be readily converted back into glucose and released into the blood when the body needs energy between meals or during periods of fasting.
Causes and Development of Insulin Resistance
The development of insulin resistance at a cellular level involves a reduced response of insulin-sensitive tissues, such as muscle, fat, and liver, to insulin stimulation. Cells can become “numb” to insulin’s signal due to defects in the insulin receptor or issues with the signaling pathways inside the cells after insulin binds.
Chronic overconsumption of processed carbohydrates and sugars is a significant dietary factor contributing to insulin resistance. This constant high intake of glucose leads to persistently elevated insulin levels, which can desensitize cells over time. A lack of regular physical activity also plays a role, as exercise enhances the body’s sensitivity to insulin and helps muscles absorb glucose more efficiently.
Body composition, particularly the accumulation of excess fat, is a major contributor to insulin resistance. Visceral fat, which is fat stored around internal organs in the abdominal area, is especially problematic. This type of fat releases substances that can directly interfere with insulin signaling in other tissues. Genetic predisposition can also increase an individual’s likelihood of developing insulin resistance. Chronic stress is another factor, as it can raise cortisol levels, a hormone that may contribute to insulin resistance.
Symptoms and Medical Diagnosis
Insulin resistance often develops without noticeable symptoms in its early stages, as the pancreas compensates by producing more insulin to keep blood sugar levels normal. However, as the condition progresses, several signs may emerge. Common symptoms include persistent hunger, especially cravings for carbohydrates, and general fatigue, particularly after meals, because cells are not efficiently receiving energy from glucose. Individuals may also experience difficulty losing weight and increased fat accumulation around the abdomen.
A visible sign associated with insulin resistance is acanthosis nigricans, characterized by dark, velvety patches of skin. These patches typically appear on the neck, armpits, groin, or under the breasts. Small skin growths, known as skin tags, can also be present.
Medical diagnosis involves several blood tests. Elevated fasting insulin levels are a key indicator, reflecting the pancreas’s increased effort to overcome cellular resistance. Fasting glucose levels may still be within the normal range in the early stages, but can become elevated as resistance worsens. The HbA1c test provides an average of blood glucose levels over the past two to three months, offering insight into longer-term glucose control. The Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) index estimates the degree of insulin resistance using fasting glucose and insulin levels.
Relationship with Metabolic Syndrome and Type 2 Diabetes
Insulin resistance is considered a cornerstone of metabolic syndrome, a cluster of conditions that collectively increase the risk of heart disease, stroke, and type 2 diabetes. The other criteria for metabolic syndrome include:
A large waist circumference (typically over 40 inches for men and 35 inches for women)
Elevated blood pressure (130/85 mm Hg or higher)
High triglyceride levels (150 mg/dL or greater)
Low levels of high-density lipoprotein (HDL) cholesterol (under 40 mg/dL for men and 50 mg/dL for women)
The presence of three or more of these conditions confirms a diagnosis of metabolic syndrome.
The progression from insulin resistance to type 2 diabetes is a gradual process. Initially, the pancreas works harder, producing higher amounts of insulin to maintain normal blood sugar levels despite the cells’ reduced responsiveness. This compensatory phase, known as hyperinsulinemia, can last for years. Over time, however, the insulin-producing beta cells in the pancreas can become exhausted from this continuous overwork. When these cells can no longer produce sufficient insulin to overcome the resistance and regulate blood sugar, glucose levels rise consistently, leading to the onset of prediabetes and eventually type 2 diabetes.