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01. Hunger and Satiety: How GLP‑1, GIP, Ghrelin, Leptin and Insulin Work Together
Why do we sometimes stop eating naturally, while at other times we want to keep going even though we have already eaten?
Food intake is regulated by a network of signals between the digestive tract, brain, pancreas and fat tissue. Some convey information about the meal just eaten, while others reflect longer-term energy stores.
In this article, we explore GLP‑1, GIP, ghrelin, leptin, insulin and glucagon. Each has a different role — their actions cannot be reduced to a single ‘hunger switch’.
Hunger, appetite and satiety are not the same
Hunger describes the need to eat. Appetite may also relate to the smell, availability or anticipated pleasure of food. Satiation helps bring a meal to an end, while satiety describes the period after eating during which we do not feel the need for another meal.
In these processes, hormonal signals interact with neural inputs and experience. Feeling hungry therefore does not reveal the level of a particular hormone or confirm a hormonal disorder.
Hormone overview: who delivers which message?
| Hormone | Main site of production | Basic role |
|---|---|---|
| GLP‑1 | Intestinal L cells | Contributes to the response to food, supports glucose-dependent insulin secretion, slows gastric emptying and influences food intake. |
| GIP | K cells, mainly in the upper small intestine | An incretin primarily involved in supporting insulin secretion after nutrient intake. |
| Ghrelin | Mainly the stomach | Contributes to stimulating hunger and food intake. |
| Leptin | Mainly fat tissue | Conveys information about energy stores and contributes to longer-term regulation of food intake. |
| Insulin | Pancreatic beta cells | Helps regulate blood glucose, its use and nutrient storage. |
| Glucagon | Pancreatic alpha cells | Supports glucose release and production in the liver, particularly when the body needs it between meals. |
This table provides a general overview. Hormonal effects depend on the body’s current state and interactions between hormones.
GLP‑1 and GIP: two incretins with different actions
GLP‑1 stands for glucagon-like peptide-1. GIP is glucose-dependent insulinotropic polypeptide. Both are incretins, intestinal hormones involved in the insulin response to nutrient intake.
Their effects are not identical. In a small randomised study in healthy volunteers, GLP‑1 administration substantially slowed gastric emptying and reduced hunger ratings. GIP administration did not show the same effect on hunger and satiety. The finding relates to a specific experiment, rather than every situation in everyday life. [1]
A natural hormone and a medicine are not interchangeable. Results from trials of medicines acting on GLP‑1 or GIP receptors cannot automatically be applied to foods or food supplements.
Ghrelin: a signal that promotes food intake
Ghrelin is produced mainly in the stomach and is often called the ‘hunger hormone’. Its role in humans is also supported by a controlled study in which ghrelin administration increased both appetite and the amount of food eaten. [2]
However, ‘hunger hormone’ is shorthand. Ghrelin is not the only reason we eat, and GLP‑1 is not simply its opposite. These signals form part of a broader network.
Leptin: information about energy stores
Leptin is produced mainly by fat tissue. Its role in appetite regulation has also been demonstrated in research involving people with rare congenital leptin deficiency, in whom replacement markedly changed food intake. This condition is fundamentally different from common obesity. [3]
Greater amounts of fat tissue are generally accompanied by higher leptin levels. However, the simple equation ‘more leptin = less hunger’ does not hold. In obesity, a reduced response to leptin is often discussed as leptin resistance. This is more complex than a lack of willpower or the effect of a single unsuitable meal.
Insulin and glucagon: managing glucose
Insulin
Helps cells, particularly in muscle and fat tissue, take up glucose and influences its processing in the liver. In insulin resistance, tissues do not respond adequately to its actions. The pancreas may initially compensate by producing more insulin. [4]
Glucagon
Helps ensure glucose availability between meals by supporting its release and production in the liver. Together with insulin, it forms part of a regulatory system that responds to the body’s changing needs.
Insulin should therefore not be described solely as a ‘fat-storage hormone’, or glucagon as a ‘fat-burning hormone’. Such labels leave out their basic physiological roles.
Why can hunger increase after weight loss?
The body adapts to changes in energy stores. In a study involving an intensive weight-loss programme, researchers observed lower leptin, higher ghrelin and increased subjective hunger after weight loss. Some changes persisted approximately a year later. [5]
This research helps explain why maintaining a lower weight can be challenging. It does not mean that everyone responds in the same way or that their metabolism is permanently ‘broken’. The study followed a specific group after a substantial dietary intervention.
What cannot be determined from feelings alone?
Sugar cravings, hunger after meals or fatigue alone do not confirm GLP‑1 deficiency, leptin resistance or insulin resistance. For example, insulin resistance and prediabetes often have no obvious symptoms, and their assessment belongs within healthcare. [4]
Likewise, increasing one hormone cannot be assumed to guarantee weight loss. When evaluating research, actual food intake, weight change, the duration of an effect and safety must also be considered.
Simply put
Hunger is more than a matter of willpower. The brain constantly processes signals about food and energy stores. Ghrelin promotes hunger, GLP-1 plays a role in satiety, and leptin signals how much energy is stored. How hungry you feel cannot tell you the level of a particular hormone or establish a diagnosis.
In the next article: diet and GLP‑1
We explore protein, fibre and meal composition. We explain what human studies show and why a measured hormonal response does not necessarily mean longer-lasting satiety or a lower body weight.
Continue to article 02: Diet and GLP-1 →Curious about what’s in food supplements?
Our Nutraceuticals Buying Guide lets you compare ingredients across the KINGRAY range and check the amounts per daily dose and any precautions for use.
- Edholm et al. (2010): Differential incretin effects of GIP and GLP‑1 on gastric emptying, appetite, and insulin-glucose homeostasis. A small randomised study in humans.
- Wren et al. (2001): Ghrelin enhances appetite and increases food intake in humans. A controlled interventional study in humans.
- Farooqi et al. (1999): Effects of recombinant leptin therapy in a child with congenital leptin deficiency. An observation in rare congenital leptin deficiency.
- NIDDK: Insulin Resistance & Prediabetes. Expert information for the public.
- Sumithran et al. (2011): Long-term persistence of hormonal adaptations to weight loss. A study of hormonal changes after weight loss.
Educational purpose: This article does not replace individual medical assessment, diagnosis or treatment. It does not recommend changing medicines independently or attempting to alter hormones with food supplements.
