Diet and nutritionInsulin and obesity — does this hormone determine weight gain?
Sources: 10 · Article: 12 590 characters
There is no single agreed answer: Ewa Dąbrowska and Bracia Rodzeń assign insulin an important role in weight gain, while Prof. David Ludwig questions whether insulin alone determines the amount of body fat.
- Ewa Dąbrowska and Bracia Rodzeń link high insulin levels with fat storage or weight gain; Ewa Dąbrowska also points to processed food and lack of exercise.
- Prof. David Ludwig describes weight gain after insulin is administered, but also writes that the brain regulates fat stores and that losing weight can become harder despite declining insulin levels.
- Ewa Dąbrowska also describes effects in both directions: excess fat can weaken the action of insulin, while a drop in insulin during fasting is said to trigger weight loss.
What the authors write
Ewa Dąbrowska
Excess insulin may shift metabolism toward fat storage, but Ewa Dąbrowska also points to processed food and lack of exercise as the main causes of obesity.
„Obesity is a hormonal disorder. Two hormones play a key role: insulin (produced by the pancreas) and cortisol (the stress hormone produced by the adrenal glands). A diet rich in processed carbohydrates (e.g. pizza, white bread, sweets) leads to a rise in insulin levels. Excess insulin can reprogram metabolism toward fat storage.”Otyłość to zaburzenie hormonalne. Kluczową rolę odgrywają dwa hormony: insulina (produkowana przez trzustkę) i kortyzol (hormon stresu wytwarzany przez nadnercza). Dieta bogata w przetworzone węglowodany (np. pizza, białe pieczywo, słodycze) prowadzi do wzrostu poziomu insuliny. Nadmiar insuliny może przeprogramować metabolizm w kierunku odkładania tłuszczu.
Bracia Rodzeń
Bracia Rodzeń describes insulin as a signal to store energy and links a higher carbohydrate intake with faster and greater weight gain.
„After eating carbohydrates, insulin levels in the blood rise significantly. Insulin is a hormone that signals the body to store energy. The more carbohydrates your food contains, the faster and more you will gain weight, develop insulin resistance, and develop other metabolic diseases.”Po spożyciu węglowodanów poziom insuliny we krwi znacznie wzrasta. Insulina to hormon, który daje sygnał do magazynowania. Im więcej węglowodanów w Twoich pokarmach, tym szybciej i bardziej przytyjesz, zachorujesz na insulinooporność i inne choroby metaboliczne.
prof. David Ludwig
Prof. David Ludwig reports that starting insulin treatment for type 2 diabetes, or overtreating type 1 diabetes, predictably leads to weight gain.
„Conversely, starting insulin treatment in type 2 diabetes or overtreating type 1 diabetes predictably causes weight gain. Part of this effect is metabolic, not simply due to differences in glucose loss in the urine [Carlson].
In animals, insulin administration causes weight gain.”Conversely, insulin initiation in type 2 diabetes or overtreatment in type 1 diabetes predictably causes weight gain. A component of this effect is metabolic, not simply differences in glucose loss in urine [Carlson].
In animals, insulin administration causes weight gain.
prof. David Ludwig
Prof. David Ludwig states that in animals, insulin can increase body fat even when food intake is restricted.
„In animals, insulin administration causes weight gain. Even when food intake is restricted to prevent weight gain, the animals still become excessively fat, showing that insulin redirects metabolic fuels to adipose tissue at the expense of lean body mass [Torbay].”In animals, insulin administration causes weight gain. Even when food intake is restricted to prevent weight gain, the animals still become excessively fat, showing that insulin redirects metabolic fuels to adipose tissue at the expense of lean body mass [Torbay].
prof. David Ludwig
Prof. David Ludwig argues that the brain, not fat tissue or the pancreas alone, regulates the amount of fat stored in the body.
„Body fatness is regulated by the brain, not by fat tissue or the pancreas. There is a vast research literature showing that the brain regulates food intake, energy expenditure, and fat tissue metabolism to regulate the size of body fat stores (10). There is no known mechanism intrinsic to fat tissue or the insulin-secreting pancreas that does this.”Body fatness is regulated by the brain, not by fat tissue or the pancreas. There is a vast research literature showing that the brain regulates food intake, energy expenditure, and fat tissue metabolism to regulate the size of body fat stores (10). There is no known mechanism intrinsic to fat tissue or the insulin-secreting pancreas that does this.
prof. David Ludwig
Prof. David Ludwig notes that losing weight becomes harder, even though weight loss itself lowers insulin levels.
„This is because weight loss itself reduces insulin levels, both between and after meals (15, 16). Yet what we observe is the opposite: weight loss becomes more difficult the more you lose, despite declining insulin levels (a negative feedback process).”This is because weight loss itself reduces insulin levels, both between and after meals (15, 16). Yet what we observe is the opposite: weight loss becomes more difficult the more you lose, despite declining insulin levels (a negative feedback process).
Ewa Dąbrowska
Ewa Dąbrowska writes that insulin levels fall during fasting, which is said to trigger processes that reduce body weight.
„During fasting, insulin levels fall, triggering processes that reduce body weight and reverse metabolic diseases. Abdominal obesity is particularly dangerous — visceral fat acts like a gland that releases pro-inflammatory substances (adipokines), which promote the development of insulin resistance and inflammation.”W czasie postu poziom insuliny spada, co uruchamia procesy redukcji masy ciała i cofania się chorób metabolicznych. Szczególnie groźna jest otyłość brzuszna – tłuszcz trzewny działa jak gruczoł wydzielający substancje prozapalne (adipokiny), które sprzyjają rozwojowi insulinooporności i stanów zapalnych.
Ewa Dąbrowska
Ewa Dąbrowska describes the relationship in the opposite direction: fats that reach cells first can block the action of insulin.
„When fats reach cells first, they block the action of insulin. If fat accumulates in the liver and muscles, insulin cannot effectively “open the door” for glucose — so it remains in the blood.
As a result, blood sugar levels rise, and the pancreas produces more and more insulin to “push” excess glucose into cells so it can be burned.”Gdy pierwsze do komórek docierają tłuszcze, blokują działanie insuliny. Jeśli dochodzi do stłuszczenia wątroby i mięśni, insulina nie jest w stanie skutecznie „otworzyć drzwi” dla glukozy – ta pozostaje we krwi.
W efekcie poziom cukru wzrasta, a trzustka produkuje coraz więcej insuliny, aby „wcisnąć” nadmiary glukozy do komórek celem jej spalenia.
Ewa Dąbrowska
Ewa Dąbrowska writes that excess fat can worsen insulin resistance, while natural carbohydrates do not cause it if they are not accompanied by excess fat.
„Even healthy fats, such as vegetable oils, can worsen insulin resistance if consumed in excess. By contrast, natural carbohydrates, such as fruit, even sweet fruit, or potatoes, do not cause insulin resistance — as long as they are not accompanied by excess fat.”Nawet zdrowe tłuszcze, np. oleje roślinne, mogą nasilać insulinooporność, jeśli są spożywane w nadmiarze. Z kolei naturalne węglowodany, takie jak owoce, nawet słodkie, czy ziemniaki, nie powodują insulinooporności – o ile nie towarzyszy im nadmiar tłuszczu.
Ewa Dąbrowska
Ewa Dąbrowska again links obesity with processed food and lack of exercise, and describes insulin as one of two important hormones.
„The main cause of obesity is an unhealthy lifestyle — above all, excessive consumption of processed food and lack of physical activity. A fruit-and-vegetable fast combined with exercise directly addresses the causes of disease: excess calories and too little exercise. Obesity is a hormonal disorder. Two hormones play a key role: insulin (produced by the pancreas) and cortisol (the stress hormone produced by the adrenal glands).”Główną przyczyną otyłości jest niezdrowy styl życia – przede wszystkim nadmierne spożycie przetworzonej żywności i brak aktywności fizycznej. Post warzywno-owocowy, połączony z ruchem, działa bezpośrednio na przyczyny chorób: nadmiar kalorii i niedobór ruchu. Otyłość to zaburzenie hormonalne. Kluczową rolę odgrywają dwa hormony: insulina (produkowana przez trzustkę) i kortyzol (hormon stresu wytwarzany przez nadnercza).
Research from PubMed · Europe PMC
We selected 3 studies with the best, positive results. This is a selection, not a full review of all research.
Total number of studies on this topic in PubMed: 21 762.
The review suggests that elevated insulin may promote an increase in fat tissue, including by inhibiting its breakdown and stimulating its storage.
Aim of the study: Lifestyle factors that increase diabetes risk are associated with elevated basal insulin levels (hyperinsulinaemia). The latter predicts later obesity in children and adolescents. A causal role of hyperinsulinaemia in adipose tissue growth is probable because pharmacological reduction of insulin secretion lowers body weight in people who are obese.
Results: Genetic inactivation of insulin gene alleles in mice also lowers their systemic insulin levels and prevents or ameliorates high-fat diet-induced obesity. Hyperinsulinaemia causes weight gain because of a physiological property of insulin. Insulin levels that are on the high side of normal, or which are slightly elevated, are sufficient to suppress lipolysis and promote lipogenesis in adipocytes. The effect of insulin on glucose transport or hepatic glucose production requires six or two times higher hormone levels, respectively. It seems justified to suggest a lifestyle that avoids high insulin levels in order to limit anabolic fat tissue activity.
Money for the studynot stated
Do the authors have ties to companies?yes — the authors reported it
Did a manufacturer help with the study?YES
Type of studydiscussion of other studies
“Not stated” does not mean nobody paid — the database does not always record it.
An animal study suggests that excess insulin may promote fat storage in the liver and adipose tissue.
Aim of the study: Genetically or experimentally produced (e.g. via lesions of the hypothalamus) obese animals have several common features, such as increased hepatic lipogenesis (resulting in fat infiltration) and increased hepatic lipoprotein secretion, together with increased adipose tissue lipogenesis.
Results: This defect is also related to hyperinsulinemia and is markedly reduced when hyperinsulinemia in obese mice is normalized. Hyperinsulinemia may thus be a key feature of obesity syndromes and may bring about most of the abnormalities observed, including the subsequent state of insulin resistance known to occur in obese animals. The cause of hyperinsulinemia in genetically obese animals is still unknown. Possible mechanisms include primary dysfunction of the pancreas and primary dysregulation of overall endocrine pancreas activity by the hypothalamus.
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studyanimal study
“Not stated” does not mean nobody paid — the database does not always record it.
The review suggests that insulin action in adipose tissue may increase its capacity to store fat, although the effect depends on the tissue.
Aim of the study: The incidence of obesity is rapidly increasing worldwide. Obesity-associated insulin resistance has long been established as a significant risk factor for obesity-related disorders such as type 2 diabetes and atherosclerosis.
Results: While enhanced insulin signaling in the liver increases hepatic fat accumulation and exacerbates dyslipidemia, enhanced insulin signaling in adipose tissue protects against obesity-related dysfunction of various organs by increasing the capacity for fat accumulation in adipose tissue and inhibiting ectopic fat accumulation. Thus, this “healthy adipose tissue expansion,” achieved by enhancing insulin sensitivity in adipose tissue but not in the liver, may be an effective therapeutic strategy for obesity-related disorders. To effectively address obesity-related metabolic disorders, the mechanisms of insulin resistance in various tissues of obese patients must be understood, and drugs that enhance insulin action must be developed. In this article, we review the potential of interventions that enhance insulin signaling as a therapeutic strategy for obesity-related disorders, focusing on the molecular mechanisms of insulin action in each tissue.
Money for the studyuniversity or foundation · Japan Society for the Promotion of Science, Japan Diabetes Society
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies
“Not stated” does not mean nobody paid — the database does not always record it.
Perspectives and opinion materials
The content below presents the authors’ opinions, interpretations and hypotheses. It is not treated as equal to scientific studies and systematic reviews.
Orthomolecular Medicine News Service Opinion material
„Vitamin C and Adipose Tissue As with all other conditions in the body, the pathophysiology of obesity relates directly to chronically increased oxidative stress and the body's response to it. Adipocytes (fat cells) increase in both number and size as they encounter more oxidative stress. [30] When sufficient VC is also not present, the pro-oxidants or toxins that make up the increased oxidative stress go unneutralized. When they remain unneutralized, the body seeks to counter their toxic impact through a compensatory mechanism.”Vitamin C and Adipose Tissue As with all other conditions in the body, the pathophysiology of obesity relates directly to chronically increased oxidative stress and the reaction of the body to its presence. Adipocytes (fat cells) increase in both number and size as more oxidative stress is encountered. [30] When sufficient VC is not present as well, the pro-oxidants or toxins comprising the increased oxidative stress go unneutralized. When they go unneutralized, the body seeks to counter their toxic impact by a compensatory mechanism.
Orthomolecular Medicine News Service Opinion material
„Obesity Hallmarks [43-46] Chronic inflammation (“adipoinflammation”) Hormonal dysregulation (leptin/insulin resistance) Mitochondrial overload & incomplete oxidation Adipose tissue hypoxia Oxidative stress Altered gut microbiome 12. Hypertension Hallmarks [47-50] Endothelial dysfunction Vascular inflammation RAAS system overactivation Oxidative stress Mitochondrial impairment in smooth muscle cells Microbiome-mediated metabolic signals 13. Cancer (Hallmarks of Cancer) Hallmarks [3, 4, 51] Sustaining proliferative signaling Evading apoptosis Reprogramming cellular metabolism Genome instability Tumor-promoting inflammation Immune evasion 14.”Obesity Hallmarks [43-46] Chronic inflammation ("adipoinflammation") Hormonal dysregulation (leptin/insulin resistance) Mitochondrial overload & incomplete oxidation Adipose tissue hypoxia Oxidative stress Altered gut microbiome 12. Hypertension Hallmarks [47-50] Endothelial dysfunction Vascular inflammation RAAS system overactivation Oxidative stress Mitochondrial impairment in smooth muscle cells Microbiome-mediated metabolic signals 13. Cancer (Hallmarks of Cancer) Hallmarks [3, 4, 51] Sustaining proliferative signaling Evading apoptosis Reprogramming cellular metabolism Genome instability Tumor-promoting inflammation Immune evasion 14.
Orthomolecular Medicine News Service Opinion material
„If this study showed positive results, it could potentially benefit millions of people worldwide with chronic inflammatory disease. [1] Metabolic syndrome Metabolic syndrome or “adiposity” is a chronic accumulation of body fat.”If this study showed positive results, this would potentially benefit millions of people world-wide with chronic inflammatory disease.[1] Metabolic syndrome Metabolic syndrome or "adiposity" is a chronic accumulation of body fat.
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