Anabolic effects of insulin on muscle fiber and adipose tissue have long been recognized, and some of the weight gain associated with insulin can be attributed to this. Increases in body weight during the first 6 months of insulin therapy are typically related to glucose control and can be primarily attributed to the decrease of glycosuria and the process of weight “regain” previously discussed. Further into treatment, there seems to be an insulin effect that contributes to weight gain and is independent of glycemic control. The addition of exogenous insulin may cause increased weight gain in patients with insulin resistance and hyperinsulinemia.

Weight gain that occurs with the initiation of insulin therapy has been reported to vary from 0.3 kg to 6.4 kg and may contribute to a patient’s reluctance to start using insulin. Weight gain occurs early — in the first weeks to months after insulin initiation — then levels off, correlating with the intensity of insulin titration. Insulin is an effective and safe agent in reducing glycated hemoglobin A1c; although its use is associated with weight gain, it is not associated with an increased risk of hypoglycemia.

Insulin therapy can cause weight gain; when insulin is started, clinicians are advised to continue metformin, SGLT2 inhibitors, and GLP-1 receptor agonists, and to stop sulfonylureas, meglitinides, and DPP-4 inhibitors because they add no further benefit and increase the risk of hypoglycemia and weight gain.

Insulins, sulfonylureas, and thiazolidinediones can promote weight gain and should be used judiciously and at the lowest possible dose. Glucose-lowering medications that promote weight loss should be prioritized.

Insulin-associated weight gain may result from a reduction of blood glucose to levels below the renal threshold without a compensatory reduction in calorie intake, a defensive or unconscious increase in calorie intake caused by the fear or experience of hypoglycaemia, or the "unphysiological" pharmacokinetic and metabolic profiles that follow subcutaneous administration. Intensive insulin therapy in both type 1 and type 2 diabetes is commonly associated with weight gain. The resulting weight gain appears to be predominantly adipose tissue in type 2 diabetes, whereas in type 1 diabetes there may be a greater contribution from lean tissue, particularly when insulin therapy is initiated in underweight individuals.

Moderate weight gain is usual after starting insulin therapy. By the time insulin was started, a high baseline A1C and insulin dose requirements were independently associated with greater weight gain, as was lower baseline BMI. A meta-analysis of randomized clinical trials indicated that weight gain was less at 1 year in those treated by basal insulin rather than by two injections a day or prandially, with no differences between the latter two regimens.

A key contributor to obesity in T1D is the weight gain that occurs with intensive insulin therapy. The nonphysiologic subcutaneous delivery of insulin in T1D results in an imbalance between the hepatic and peripheral effects of insulin. This can lead to peripheral hyperinsulinemia, which could contribute to both weight gain and hypoglycemia.

The key mechanisms causing insulin-associated weight gain (IAWG) appear to be the reduction of glycosuria, "defensive snacking" against hypoglycaemia, "catch-up" weight gain and the un-physiological route of administration of exogenous insulin. The potential causes for this weight gain include: an increase in energy intake linked to a fear of hypoglycaemia, a reduction in glycosuria, catch-up weight, and central effects on weight. This suggests an interplay between hypothalamic inflammation and central insulin resistance resulting in a suppression of insulin signalling affecting anorexigenic hormone release, energy homeostasis, and subsequently peripheral insulin resistance.

All regimens were associated with approximately 30% increased probability of achieving HbA1c target, 1 kg greater weight gain, and a borderline increase in the risk of severe hypoglycaemia. Complex insulin regimens provide modest glycaemic benefits over basal insulin but are associated with greater weight gain and a suggested higher risk of hypoglycaemia.

In both types of diabetes, the excess weight gain with intensified insulin therapy compared with conventional insulin or sulfonylurea remains modest: 2.6 kg over 7.5 years in the Stockholm study (type 1 diabetic patients) and 1.7 kg when compared to glibenclamide over 10 years in the UKPDS (type 2 diabetic patients). Patients who gain the most weight after insulin initiation are those who had the worst metabolic control before intensification, greater weight loss prior to insulin, and in type 1 diabetes a family history of type 2 diabetes. This suggests that most of the weight gain observed after insulin initiation is a "catch-up" weight re-gain.

Mechanisms for this weight gain are complex. Insulin 1) reduces glycosuria and its caloric expenditure; 2) stimulates the storage of fatty acids into triglycerides in adipose tissue, thus favoring an increase in adipose mass; 3) yields a positive nitrogen balance through an inhibition of muscle proteolysis, thus favoring an increase in lean mass. Thus, insulin therapy is associated with weight gain through both increased fat mass and increased lean body mass.

In type 1 patients, insulin led to the most important weight gain, but it was fat-free, with a major benefit on HbA1c. Insulin-induced body weight gain is not univocal: insulin restores or protects lean mass in its less controversial indications, whereas it leads to fat accumulation in type 2 patients with isolated failure of oral agents. In type 2 patients with residual endogenous insulin secretion, the insulin-induced weight gain appears to be mainly due to an increase in fat mass.

Over 6 months the control group gained 4.9 (SD 3.6) kg (P < 0.001), whilst the intervention group maintained their weight (−0.6 (SD 5.1) kg; NS). The difference in weight change between the groups was 5.5 kg (P < 0.001). The present study demonstrates that weight gain is not an inevitable consequence of starting insulin therapy, but attenuation of the weight gain requires a high level of intervention.

Insulin use is associated with hypoglycemia and weight gain. Insulin use, particularly in high doses, is associated with weight gain. ADA guidelines and AACE/ACE guidelines suggest minimizing the use of concomitant medications that may cause weight gain when treating patients with type 2 diabetes.

Almost all those with type 2 diabetes who start insulin therapy or intensify it gain weight, which may potentially diminish the prognostic advantage of improved glycaemia. Insulin treatment is associated with weight gain in most randomized controlled trials comparing insulin with other glucose-lowering therapies. The body of evidence presented in this review indicates that glycaemic management with exogenous insulin replacement is of a much higher priority than weight gain.

The mechanisms of this weight gain are incompletely understood, but reduction of energy lost by glucosuria and reduction of energy needed for glucose production are main determinants. Weight gain is a frequent consequence of intensive insulin therapy in both type 1 and type 2 diabetic patients. This insulin-induced weight gain is mainly adipose tissue in type 2 diabetics, whereas in type 1 it may be partly lean tissue, especially when insulin is initiated in thin patients.

It is concluded that type 2 diabetic subjects, especially on insulin treatment, gain weight due to unadvised and increased caloric intake. Type 2 diabetic subjects on insulin therapy showed significant weight gain compared to non-insulin users, and this weight gain was related to increased caloric intake. Insulin-associated weight gain is a frequent clinical problem in type 2 diabetes and may be partly preventable by appropriate dietary counseling.

Insulin is anabolic hormone that plays a role in inhibiting protein catabolism, stimulating lipogenesis, and slowing basal metabolism, resulting in increased fat accumulation. These effects are enhanced by exogenous insulin administration, since exogenous insulin imperfectly mimics endogenous secretion. While endogenous insulin has its first pass to the liver through the portal vein to suppress gluconeogenesis, exogenous insulin circulates systemically first and disproportionately affects muscle and adipose in comparison to the liver.

Starting insulin was associated with weight increase, independent of pre-insulin weight change (β-adjusted 1.228, p < .001). Initiation of insulin therapy was independently associated with weight increase; however, overall effect on weight was small and subject to substantial variation.

The 2026 Standards of Care were published as a supplement to the January 2026 issue of Diabetes Care. The Standards continue to emphasize weight management in diabetes care and include updated guidance on obesity treatment and medication selection.

Our results suggest that repeated iatrogenic hypoglycemia leads to weight gain, and that such weight gain is associated with a multifaceted deficit in metabolic regulation rather than a chronic increase in caloric intake. Weight gain as a result of insulin therapy is a consistent finding of major trials and is often greater than that seen with other treatment regimens. We conclude that episodes of hypoglycemia, followed by defensive eating and hormonal counterregulation, may be an important mechanism linking intensive insulin therapy to weight gain.

After adjusting for age, race, sex, baseline weight, intervention status, and change in A1C, insulin users had 2.5 kg less weight gain than noninsulin users (P = 0.033). Insulin therapy in the treatment of diabetes has been associated with weight gain in both clinical trials and clinical practice, but in this cohort of well-controlled type 2 diabetes patients participating in a weight maintenance trial, insulin use was not associated with greater weight gain. These findings suggest that when lifestyle interventions are in place, insulin-treated patients can maintain weight as well as noninsulin-treated patients.

All study groups except those allocated to insulin alone experienced a modest decline in weight; the mean weight change from baseline was −3.2 lb for placebo alone, −4.1 lb for metformin alone, and −1.6 lb for metformin and insulin, while allocation to insulin and placebo metformin was associated with a nonsignificant 0.5-lb weight gain (+0.2%). Weight gain of 5% or more of baseline was more common among those allocated to insulin compared with no insulin (22 vs 7, P = .01).

Long-term studies of insulin-treated patients with type 2 diabetes suggest that the weight such patients reach is asymptotic, and that most weight gain occurs during the first 3 years. We conclude that insulin therapy does not itself induce weight gain in patients with type 2 diabetes, but that weight gain results from the alleviation of glycosuria and the associated improvement in metabolic control. Insulin-treated patients with type 2 diabetes attained similar body weights to those of non-diabetic control subjects, indicating that insulin restores normal weight rather than causing obesity.

The causes of weight gain in people with type 1 diabetes are thought to be primarily related to exogenous insulin replacement therapy, which (despite continuous progress) remains unphysiological. Subcutaneous administration of insulin leads to peripheral hyperinsulinaemia and may promote weight gain. Weight gain and obesity are increasingly prevalent in people living with type 1 diabetes, in part due to intensive insulin treatment and modern therapies.

Mean estimated change in body weight from baseline ± standard error (SE) was −1.05 ± 0.23 kg for Diet+IDet and −0.56 ± 0.23 kg for IDet alone. Estimated mean difference was 0.49 kg (95% CI −0.15; 1.13, P = 0.132). This study suggests that a modest dietary intervention plus basic lifestyle advice, compared with basic lifestyle advice alone, resulted in similar weight change, efficacy, safety and tolerability when initiating insulin detemir once daily in overweight or obese insulin-naïve individuals with T2D.

Consistent with these effects, states of increased insulin action (such as insulin-producing tumors, initiation of insulin treatment of type 2 diabetes or overtreatment of type 1 diabetes) are predictably associated with weight gain. Together, these data suggest that excessive amounts of circulating insulin can promote excessive weight gain. This complements results from large cardiovascular outcome trials in people with type 2 diabetes that found insulin therapy causes weight gain.

The lipogenic effect of insulin with subsequent increase in fat mass may be the primary cause of this weight gain that can be attenuated by increases in activity levels. In type 1 diabetes mellitus, intensive insulin therapy is associated with weight gain, which may lead to obesity. Potential causes of this weight gain include the anabolic and lipogenic effects of insulin and defensive eating because of fear of hypoglycemia.

During 24 months of insulin treatment, obese patients gained significantly less body weight than normal-weight and overweight patients, while achieving clinically similar glycaemic benefits. The data suggest that baseline BMI category influences the extent of weight gain in insulin-treated patients with type 2 diabetes.

Medications for glucose-lowering or medications for comorbid conditions that are associated with weight gain should be avoided, if possible.

People who take insulin often gain weight. Insulin can cause weight gain when the cells absorb too much glucose and the body converts it to fat. Improved blood sugar control with insulin reduces loss of glucose in the urine; instead, more calories are stored, which can lead to weight gain if food intake is not adjusted. Weight gain from insulin therapy can be minimized with healthy eating and regular physical activity.

The ADA Standards emphasize weight management in diabetes, including weight loss or prevention of weight gain, and recommend intensifying treatment to achieve glycemic and weight-loss goals in people with type 2 diabetes.

Initiating insulin pump therapy in individuals with type 2 diabetes might lead to weight gain. Results indicated no significant difference in weight gain between groups: the control group gained an average of about 3 kg, while the intervention group gained about 3 kg (P = 0.xx). An approximate weight gain of 1 kg per 1% HbA1c reduction can be anticipated following intensified insulin treatment.

Weight gain can be a typical side effect of insulin therapy. When you start insulin therapy and begin getting your blood sugar under control, the glucose in your body is absorbed and stored. This causes weight gain if the amount you eat is more than you need for the day. Other factors that contribute to insulin-related weight gain include defensive eating to prevent hypoglycemia and reduced glycosuria once insulin is started.

New: Care goals should include weight loss or prevention of weight gain, minimizing progression of hyperglycemia, and attention to cardiovascular risk and associated comorbidities.

Why does insulin treatment promote weight gain? Various mechanisms have been described: calorie conservation – insulin therapy can, in some cases, restore blood glucose levels to below the renal threshold for glucose excretion, leading to an improved conservation of ingested calories; compensation for hypoglycaemia or ‘defensive snacking’; and deranged pharmacodynamic and metabolic profile due to subcutaneous insulin delivery. Therefore in insulin therapy via the subcutaneous route, the liver is ‘underinsulinised’ and the periphery ‘overinsulinised’, exposing the systemic circulation to increased metabolic effects associated with circulating insulin. These factors together can promote weight gain in people receiving insulin.

These studies show that glycaemic control can be better with pre-mixed rather than basal insulin, but with higher risk of hypoglycaemic episodes and weight gain. In our cohort comparing two different insulin initiation regimens in patients with type 2 diabetes, no difference was seen in terms of incidence of hypoglycaemia or weight gain between the two regimens.

The American Diabetes Association’s 2023 Standards of Care emphasize supporting higher weight loss goals when appropriate and considering access to newer medications.