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Not sugar, but fat is the cause of overweight

Calorie retriction is needed in fat-rich diets to compensate for the whole fat, otherwise you would increase. It is possible to reduce fat-rich diets such as low carb or ketogen by reducing its calories, but a high-fat diet increases insulin resistance, increases cholesterol levels and causes cardiovascular diseases. You can also lose weight without a calorie restriction by feeding yourself very low in fat to avoid storing new fat and moving to boost your metabolism so that mitochondria effectively burn fat. Sugar is not converted into fat, except for a calorie excess, or if fat production in the liver is promoted by insulin resistance or fatty liver. The Single copy Sugar, which is actually converted into triglycerides in the liver, is isolated fructose (e.g. hundreds of grams of fruit sugar powder).

Saturated fat intake and resistance insulin in men with coronary artery disease. The Stanford Coronary Risk Intervention Project Investigators and Staff
1991: The absorption of saturated fatty acids is positively related to the BMI, the absorption of carbohydrates negative. An attractive explanation for this observation is that food fat is converted more efficiently into body fat than carbohydrates: food fat can be stored in the fatty tissue with a metabolic energy requirement of 3% of the absorbed fat calories, while the metabolic energy requirement for the storage of carbohydrates in fat requires 23% of the absorbed carbohydrate calories. In addition, the saturated fatty acids, regardless of whether they make us thick, can contribute to the development of insulin resistance and its clinical consequences. (Since the conversion of small sugar molecules into long fatty acids is complicated and wastes energy, the body burns carbohydrates and primarily stores food fats.)

Regulation of endogenous fat and carbohydrates in relation to exercise intensity and duration
1993: The energy supply depends on the intensity of the physical load. With lower physical stress (e.g. walking), you burn more fat and less sugar. With high physical stress (e.g. sports), you burn more sugar and less fat.

A low-fat diet and/or strenuous exercise ages the IGF axis in vivo and reduces prostate tumor cell growth in vitro
2003: The one group has fed up normally and made intensive sports 1 hour a day. The other group has fed vegans and had only slight movement, such as walking. After 14 years, the group with strong physical activity was still overweight and the vegan group has reached an ideal body weight.

Dietary trans fatty acids and composition of human atheromatous plaques
2004: The fatty acids from the oils are found both in the atherosclerotic plaque and in the fatty tissue. Oils thus promote overweight, damage the vessels and promote the development of atherosclerosis.

A two-year randomized weight loss comparing a vegan diet to a more moderate low-fat diet
2007: Vegan diet against the National Cholesterol Education Program (NCEP), a diet regarding weight loss: The vegan diet is gaining.

Effects of 7 days on ad libitum low-fat vegan diet: the McDougall Program cohort
2014: Vegans who fed up low-fat and rich in carbohydrates and were allowed to eat as much calories as they wanted took off.

Obesity Energetics: Body weight regulation and the effects of Diet Composition
2017: Meta-analysis of 32 Isocaloric Metabolic Ward Studies: “‘Calories in, Calories out’ is scientific nonsense.” Weight changes are accompanied by an imbalance between calorie intake and consumption. This fact is often misinterpreted in such a way that obesity is caused by obesity and laziness, so that people are simply advised to eat less and move more. However, various components of the energy balance are dynamically connected to one another, and weight loss is counteracted by opposite physiological processes. Our meta-analysis revealed that both energy consumption and fat loss were greater in low-fat diets. (The less fat, with the same number of calories, the more you decrease.)

Will sugar be converted into fat? De-novo-lipogenesis (reformation of fatty acids):

Glycogen storage capacity and de novo lipogenesis during massive overfeeding in man
1988: It was checked how carbs are used in overfeeding. The glycogen stores of the 3 male subjects were emptied before the 7-day carbohydrate feed began.Large numbers from the graphic:Date 1: 400 g of carbohydrates were burned.Day 2: 500 g of carbohydrates were burned and 100 g were converted into fat.Day 3: 500 g of carbohydrates were burned and 200 g were converted into fat.Day 4: 500 g of carbohydrates were burned and 250 g were converted into fat.Day 5: 500 g of carbohydrates were burned and 450 g were converted into fat.Day 6: 500 g of carbohydrates were burned and 450 g were converted into fat.Day 7: 500 g of carbohydrates were burned and 500 g were converted into fat. First, the glycogen stores are enlarged before carbohydrates are converted into fat.

De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women
2001: 8 slim and 5 overweight women received meals that covered their daily calorie requirements and received 50% additional calories in the form of 27.3% sugar (saccharose or glucose) and 22.7% fat (oil or butter). During the 4-day overfeed, the test subjects received 1398g carbohydrates, burned 1280g, resulting in a carbohydrate balance of 115g.Fat production by the De-novo-Lipogenesis was only 4g. The fat supply during this period was 512 g, of which 233 g were burned, so that all subjects had a fat balance of 278 g.“The De-novo Lipogenesis does not contribute significantly to the overall fat balance.”(According to a calorie surplus, sugar hardly contributes to weight gain. About 90-97% of the fats stored in the body are due to the fatty acids from the food.)

Not sugar, but fat (and cholesterol) is the cause of and. A high-fat diet leads to insulin resistance and fat liver, which in turn promotes the de-novo lipogenesis in the liver, so that sugar is increasingly converted into fat. One of the over 40 studies:

Pathogenesis of metabolic syndrome: The importance of ectopen fat deposits in liver and skeletal muscles
2005: Fat causes metabolic syndrome.Figure 1: The mitochondrial dysfunction in the skeletal muscles of descendants of type 2 diabetics restricts the fatty acid oxidation capacity. Propagated fatty acid metabolites lead to the occurrence of insulin resistance and a subsequent reduced glucose absorption (1). Fatty acids and cytokines released from the fatty tissue also favor insulin resistance of skeletal muscles (2). Compensatorically, an increased distribution of insulin from the β cells of the pancreas (3). Hyperinsulinemia, however, promotes de-novo-lipogenesis in the liver, although the glucose production of the liver itself can no longer be suppressed by the increased insulin levels (“mixed hepatic insulin resistance” [4]). Fatty acids and cytokines increasingly released from the fatty tissue also promote the formation of a fatty liver and the hepatic insulin resistance (5). Finally, the pancreatic β-cells are also damaged by the increased circulating fatty acids (“Lipotoxicity” [6]), and in the case of declining insulin secretion, a manifest diabetes occurs.